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Immunologic Diseases


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In this disease, patients cannot develop B cells. They do not have Igα or Igβ which normally associate with the intracellular tyrosine kinases for BCR-signaling. As a result, they cannot signal to the cell to undergo light chain rearrangement, and there is NO BCR. So: No mature B cells.
Allergic Rhinitis
IgE hypersensitivity reaction (Type I hypersensitivity rxn)
Why would you give shots of an allergen to someone suffering from allergies?
Gradually increase the dose of allergen over time. Gradually there is a decrease in IgE and an increase in IgG antibodies in response to the allergen. This results in decreased eosinophils and basophils.
Amyloidosis Type II
Associated with Rheumatoid Arthritis. According to Wikipedia, the amyloid A protein is an acute phase protein associated with chronic inflammation. Deposits physically disrupt tissue architecture. Amyloidosis is thus a disease characterized by extracellular accumulation of amyloid in various organs and tissues of the body. Secondary amyloidosis occurs in association with another chronic inflammatory disease like RA. The organs chiefly involved are the liver, spleen, and kidneys, and the adrenal glands less frequently.
Ankylosing Spondylitis (Student Definition)
Progressive autoimmune inflammatory disease involving widespread and uniform spondylitis as well as sacroiliitis. Begins in early adulthood, primarily in males. Peripheral joints are NEVER involved. Leads to postural changes, compromise of chest expansion. Patients' hips are fixed so they must stand with bent knees. 25% get scarring of the iris (uveitis).
Ankylosing Spondylitis (Wikipedia Definition)
Chronic, painful, progressive autoimmune inflammatory arhtritis primarily affecting the spine and sacroiliac joints, causing eventual fusion of the spine (bamboo spine). It is a member of the group of autoimmune spondyloarthropaties with a probable genetic predisposition. Causes anterior uveitis, causing eye pain and photophobia. During acute inflammatory periods patients will show increased concentration of C reactive protein (CRP) and an increase in the erythrocyte sedimentation rate (ESR). Over 95% of ppl with AS are HLA-B27 positive. AS may be accompanied by dactylitis or enthesitis. Also affect the heart, lungs, colon, and kidneys. TNF alpha and IL-1 are implicated in ankylosing spondylitis. Treated with NSAIDs, cyclosporin, methotrexate, and TNFalpha blockers such as Infliximab.
Anti-inflammatory Medications
An example is anti-TNF-α Ab to lessen graft rejection.
Why would you treat a patient with Abs to T cells?
Hope would be to bind TCRs and inactivate the T cells.
Arthus Reaction
Arthus Rxn is a type III hypersensitivity rxn, which is immune complex mediated and involves the deposition of an Ag-Ab complex in vascular walls, serosa, and glomeruli. If an animal or patient is previously sensitized to an Ag (has circulating Abs), intradermal injection of the antigen will result in local vasculitis due to deposition of immune complexes in dermal blood vessels. Activation of complement and recruitment of PMNs ensue resulting in an inflammatory response. "Serum Sickness" is associated with Type III hypersensitivity rxns.
Atopic Dermatitis
Also called "eczema." Atopic dermatitis results when the skin of an affected person reacts to irritants, food and air allergens and becomes red, flaky, adn very itchy. Often occurs together with other atopic diseases such as hay fever, asthma, and conjunctivitis. Example of type I hypersensitivity. Patients with adoptic dermatitis have high expression of IL-4 and IL-13. They have a tendency towards TH2 responses (as opposed to TH1) and there is an IgE hypersensitivity rxn in which the skin is infiltrated by T lymphocytes.
Bone marrow transplant carries the risk of what viral infection?
EBV, because there are no T cells to keep the virus dormant.
What causes Burkitt's Lymphoma?
EBV viral antigen. Immunosuppresion is required for Burkitt's lymphoma to result. Children affected with the disease often have had chronic malaria which reduces resistance to the virus.
C1q deficiency predisposes individuals to which autoimmune disease?
C1q deficiency predisposes individuals to Systemic Lupus Erythematosis (SLE). Individuals with C1q deficiency have increased deposition of debris in the kidneys (have trouble clearing immune complexes because they are not opsonized properly) and have increased production of auto-Abs because apoptotic debris is not cleared efficiently. C1q normally binds to IgM and IgG Abs or to pathogen surfaces directly.
What disease results from a deficiency of the C2 component of complement?
A disease resembling SLE but without glomerulonephritis.
What is the purpose of a calcineurin inhibitor?
Decreases IL-2 expression. Calcineurin is a protein phosphatase responsible for activating transcription of IL-2, which stimulates the growth and differentiation of T cells. It is inhibited by cyclosporin and tacrolimus. Calcineurin dephosphorylates NFATc, a transcription factor which can then go into the nucleus and turn on genes involved in IL-2 synthesis. Used to reduce risk of graft rejection.
What is Chediak-Higashi Syndrome?
It is a rare childhood autosomal recessive disorder which arises from a mutation in the lysosomal trafficking regulator gene, LYST. It is a disease with impaired bacteriolysis due to failure of phagolysosome formation. As a result of disordered intracellular trafficking there is impaired lysosome degranulation with phagosomes, so phagocytosed bacteria are not destroyed by the lysosome's enzymes. In addition, the secretion of lytic secretory granules by cytotoxic T cells i also affected. Leads to susceptibility to infections, abnormalities in nuclear structure of leukocytes, anemia, and hepatomegaly. Also associated with a syndrome that causes hypopigementation of the skin adn hair and can cause a fatal hemophagocytic syndrome for which the only cure is bone marrow transplantation (Albinism partial immunodeficiency).
Crohn's Disease (Inflammatory Bowel Disease)
Associated with an increase in IgG2. IBD occurs when the immune system contributes to damage of the GI tract by causing inflammation. Prevalence in Northern Europe is 27-48/100,000. Associated with inflammation of the terminal ileum (as well as the rest of the GI tract). Causes abdominal pain, diarrhea, etc. as well as systemic symptoms of fever, weight loss, and growth failure. Can also cause uveitis or episcleritis. Inflammation may be transmural, deep into the tissues. Intestinal stenosis is common. Associated with Th1 response. Can have granulomas. Disease has a bimodal distribution. Tends to strike people in their teens and twenties, and people in their fifties through seventies. Mutations in a gene called NOD2 are associated with Crohn's disease.
Complement Inhibitor Deficiency
Renders patients susceptible to bacterial infections.
Why are corticosteroids administered in allograft recipients?
To reduce the risk of rejection.
To what diseases are patients deficient in CR3 and CR4 susceptible?
Pyrogenic infections and infections by Neisseria gonorrhea and Neisseria meningitidis.
Common Variable Immunodeficiency (CVID)
Characterized by a normal B cell count with NO Ig in the serum. This results either from defects in the B cells or from too much T cell suppression. Low levels of IgG, IgA, and/or IgM. Treatment is usually IvIg. Typical patient is between age 20 and 40 and both males and females are equally affected. 20% of patients are diagnosed in childhood.
Di George Syndrome
These patients lack a thymus! Due to a deletion of chromosome 22q11. As a result they have NO T cells.
Diffuse Infiltrative Lymphocytosis Syndrome (DILS)
This is caused by CD8+ T cell response. This is a disabling autoimmune disease with auto-Abs. It is normally associated with good long-term nonprogression, although it can cause B cell lymphoma.
EAE (Experimental Autoimmune Encephalomyelitis)
EAE is an animal model of multiple sclerosis. These mice have the BBB disrupted, and lymphocytes are exposed to antigens from which they are normally sequestered. As a result, there can be an attack of brain auto-antigens.
EBV is a herpesvirus. Uses CR2 (CD21) on B cells to gain entry to B cells via the gp350/gp220 part of the viral envelope, via receptor-mediated endocytosis. EBV is a dsDNA virus that can cause B cell lymphoma or nasopharyngeal carcinoma. Can cause mononucleosis: fever, lymphadenopathy, and pharyngitis. EBV integrates its DNA into the host genome which allows B cell proliferation independent of T cell help. Only produces leukemia in immunocompromised patients. EBV also causes Burkitt's lymphoma when associated with malaria infection.
Condition occurring at the insertion of muscles where recurring concentration of muscle stress provokes inflammation with a strong tendency toward fibrosis and calcification. T cell infiltration results in a combination of bony erosion and the creation of "lover's heel" as in Reiter's syndrome.
Factor H or Factor I deficiency results in what?
Factor H is a glycoprotein that regulates the activity of complement factor C3b; a deficiency results in the lack of inhibition of the alternative hemolytic pathway leading to continuous activation and consumption of factor C3 (hemolytic uremic syndrome). Patients become susceptible to bacterial infection as a result of C3 deficiency, because they lack complement.
Felty's Syndrome
Rheumatoid arthritis with splenomegaly and leukopenia. Rheumatoid factor positive. Complications include recurrent infections (due to lack of PMNs), hyperplenism resulting in thrombocytopenia, etc.
Freund's Adjuvant
Administered along with antigen to cause a TH1 mediated IgG production. Freund's adjuvant consists of oil, water, and killed mycobacteria.
Graft vs. Host Disease (GVHD)
GVHD is a common complication of allogeneic bone marrow transplantation in which functional immune cells in the transplanted marrow recognize the recipient as "foreign" and mount an immunologic attack. After bone marrow transplantation, T cells present in the graft, either as contaminants or intentionally introduced into the host, attack the tissues of the transplant recipient after perceiving host tissues as antigenically foreign. The T cells produce an excess of cytokines including TNF alpha and IL-1. Classically, acute graft-versus-host-disease is characterized by selective damage to the liver, skin and mucosa, and the gastrointestinal tract.
Hepatitis B Vaccine
20% of individuals will not respond to the Hep B vaccine because of their particular HLA haplotypes.
Hereditary Angioneurotic Edema
A relatively rare form of edema characterized by onset, usually in adolescence, of erythema followed by edema, involving the upper respiratory or GI tracts, associated w/ either a deficiency of C1 esterase inhibitor or a functionally inactive form of the inhibitor. There are 2 clinically indistinguishable forms: type I, in which the serum level of C1 esterase inhibitor is low (up to 30% of normal) and type II, in which the level is normal or elevated. There is uncontrolled activation of early complement components and production of a kininlike factor that induces the angioedema; death may occur from upper respiratory tract e. and asphyxia. Inheritance is autosomal dominant, caused by mutation in the C1-esterase inhibitor gene (C1NH) on chromosome 11q. There is no inhibition of kallikrein and unchecked formation of kinin which results in swelling.
HIV patients are at risk for EBV lymphoma, Kaposi sarcoma and squamous cell carcinomas. Gp120 and gp41 env proteins allow binding and fusing with the cells. HIV is a retrovirus w/LTR, a promoter region which allows for viral gene transcription. CCR5 or CXCR4 are req'd for viral entry. Gp120 binds to CD4 and either CCR5 or CXCR4. Gp120 mutates a bit to become R4 tropic, at which point it invades naive T cells. Mutates and escapes CD8 control by reducing MHC I expression.
Less virulent strain of the virus.
HTLV (Human T Cell Leukemia Virus)
Binds to CD4+ cells and immortalizes them. Transcription factors act as promoters of viral genes and T cell genes like IL-2 and CD25 (IL-2 receptor). Upregulates IFN-gamma and colony stimulating factor.
Hyper IgM Syndrome
X Chromosome Linked. LOTS of IgM. Not lots of the other Igs. Due to mutation in CD40, CD40L, or AID. No somatic hypermutation or class switching because no germinal centers develop so you only see low affinity IgM. Can give sCD40L to correct.
IgA Deficiency
Most common Ig deficiency. Patients are mainly healthy. Shown when patient receives a blood transfusion and has anti-IgA Abs, as the body makes IgE against donor IgA. These patients have a high incidence of respiratory tract and GI infections. They have a tendency towards autoimmunity and allergy.
Why would you give patients inosine monophosphate?
Inosine monophosphate is an inosine nucleotide. (Hypoxanthine-guanine phosphoribosyltransferase converts hypoxanthine to IMP.) IMP inhibits guanine nucleotide synthesis and thereby decreases risk of graft rejection.
Karposi Sarcoma
KS can occur among transplant patients, in whom the tumor can disseminate. Stopping immunosuppression can eliminate KS but also can cause rejection of the transplanted organ. In KS associated with immunodeficiency or immunosuppression, treating the cause of the immune system dysfunction can slow or stop the progression of KS.
Mutation in B2 integrin (CD18), a component of LFA-1 and MAC-1. Leukocytes can't bind to the endothelium and we get recurrent bacterial, fungal infections and problems with wound healing.
Mutation in sialyl-Lewis X on the endothelium which binds PMN selectins. Results in recurrent bacterial and fungal infections due to problems with PMN trafficking to infection sites.
A chronic granulomatous infection caused by Mycobacterium leprae affecting the cooler body parts, especially the skin, peripheral nerves, and testes. Leprosy is classified into two main types, lepromatous and tuberculoid, representing extremes of immunologic response. Tuberculoid form means that the bacteria are surrounded by a granuloma (DTH). TH1 cytokines are made (IFN-gamma and IL-2). The lepromatous form of leprosy means that systemic bacteria are not contained. There is a TH2 response generated which is NOT effective.
Leukocyte Adhesion Deficiency
an inherited disorder (autosomal recessive) in which there is a defective CD18 adherence complex that disturbs chemotaxis. It is characterized by recurrent bacterial pyogenic infections and impaired wound healing. The disease is due to the absence of CD18, which is part of LFA-1, MAC-1, CR3 and CR4. Phagocytosis is impaired. There is delayed sloughing of the umbilical cord in newborns.
MAC Deficiency
Deficiency in complement C5, C6, C7, C8, or C9. Results in an inability to defend oneself against Neisseria infections (gonorrhea or meningitis).
Tumor infiltrating lymphocytes (TILs) recognize melanoma antigens. CD8+ T cells are unable to kill the tumor cells. IgM Abs are made against the tumor because there is no T-cell help given to induce class switching.
Multiple Sclerosis is mediated by what class of lymphocytes?
CD4+ T cell mediated. Common demyelinating disorder of the central nervous system, causing patches of sclerosis (plaques) in the brain and spinal cord; occurs primarily in young adults, and has protean clinical manifestations, depending upon the location and size of the plaque; typical symptoms include visual loss, diplopia, nystagmus, dysarthria, weakness, paresthesias, bladder abnormalities, and mood alterations; characteristically, the plaques are “separated in time and space” and clinically the symptoms show exacerbations and remissions. In MS, certain T cells trigger inflammatory processes when they encounter myelin, stimulating other immune cells and soluble factors like cytokines and antibodies. Normally, there is a tight barrier between the blood and brain, called the blood-brain barrier, built up of endothelial cells lining the blood vessel walls. The inflammatory processes triggered by the T cells create leaks in the BBB which cause a number of other damaging effects such as swelling, activation of MFs, and more activation of cytokines and other destructive proteins such as matrix metalloproteinases. The final result is destruction of myelin, called demyelination.
How does an mTOR inhibitor help lessen risk of graft rejection?
mTOR regulates translation and cell division. Sirolimus inhibits the response to IL-2 by binding to the cytosolic protein FK-binding protein 12 (FKBP12).The sirolimus-FKBP12 complex inhibits the mammalian target of rapamycin (mTOR) pathway through derepression of PP2A, resulting in inhibition of lymphocyte proliferation. As impaired wound healing is a possible side effect of Sirolimus, some transplant centers prefer not to use it immediately after the transplant operation, and start to give it after a period of weeks or months. Its optimal role in immunosuppression has not yet been determined.
Mucosal Immunotherapy
Used to treat autoimmune disease in nonmucosal tissue by tolerizing to downregulate immune system activity.
Mucosal Vaccines
Must stimulate the MALT to be effective. Nonreplicating antigens are not good at creating long-lasting responses. Must give an antigen conjugated to cholera toxin, for example, to get a good response.
Multiple Myeloma
B cell malignancy of plasma cells). Single clone in the bone marrow is transformed. IL-6 dependent. Causes bone destruction. LOTS of Ab in blood and urine. Elevated calcium, anemia, bone lesions, & renal failure. Bone disease is due to proliferation of tumor cells and release of IL-6, also known as osteoclast activating factor (OAF), which stimulates osteoclasts to break down bone. These bone lesions are lytic in nature and are best seen in plain radiographs, which may show a "punched-out" resorptive lesions. The breakdown of bone also leads to release of Ca2+ into the blood, leading to hypercalcemia and its associated symptoms. The anemia found in myeloma is usually normocytic and normochromic. It results from the replacement of normal bone marrow by infiltrating tumor cells and inhibition of normal RBC production (hematopoiesis) by cytokines.
Oral Antigen Administration
Tolerance develops when antigens are first presented orally. Results in anergy of T cells, clonal deletion and selective expansion of T cells making immunosuppressive cytokines.
Paroxysmal Nocturnal Hemoglobinuria
Normally neither nocturnal nor paroxysmal - ongoing hemolysis is much more common. Complement inhibitory products are unable to attach to the cell surface. DAF and CD59 do not attach and cannot prevent binding of activated complement. Unregulated complement causes much damage to RBCs and platelets. A common finding in PNH is the presence of breakdown products of RBCs (hemoglobin and hemosiderin) in the urine. [A molecule called PIGA is needed to make a cell membrane anchor for proteins called GPI (glycosylphosphatidylinositol). X-linked gene. If a mutation occurs in this gene then PIGA may be defective, which leads to a defect in the GPI anchor. When this mutation occurs in a bone marrow stem cell, all of the cells it produces will also have the defect. Several of the proteins that anchor to GPI on the cell membrane are used to protect the cell from destruction by the complement system. The complement system is part of the immune system and helps to destroy invading microorganisms. W/o the proteins that protect them from complement, RBCs are destroyed. The main proteins which carry out this function are CD16, CD55 and CD59.
Pemphigus Vulgaris
Pemphigus is an autoimmune disorder that causes blistering and raw sores on skin and mucous membranes. MHC II autoimmune disease associated with HLA-DR4. Auto-Ab binds to prickle cells, directed at desmoglein 3, and disrupts the integrity of inter-keratinocyte adhesion. To restate, disease occurs when antibodies attack Desmoglein 3, a protein that keeps cells bound together. Thus, cells simply fall apart, causing skin to slough off. Although pemphigus vulgaris may occur at any age, it is quite rare in children, and most common in the middle aged and elderly.
Why would you intentionally give somebody Pertussis Bacilli?
Adjuvant administered with antigen, causes an IgE reaction for TH2 direction. This is the germ for the whooping cough.
Poison Ivy
DTH Reaction. Type IV. Contact dermatitis. CD8+ T cell mediated.
Psoriasis and Psoriatic Arthritis
It is thought that T cells (which normally help protect the body against infection) become active, migrate to the dermis and trigger the release of cytokines (TNFα in particular) which cause inflammation and the rapid production of skin cells. T cells invade the skin because keratinocytes are presented on MHC Class I. Cytokines are produced by the T cells which retard keratinocyte differentiation. 15% of these patients develop psoriatic arthritis, which attacks the DIP joints. Inflammation and trauma initiates the T-cell response and the auto-Ag process ensues. The autoimmune reaction then transitions to the joints and fibrosis results.
Ragweed Allergy
IgE mediated type I hypersensitivity reaction. Development depends on HLA genetics.
Reiter's Syndrome (Reactive Arthritis)
Transmitted via enteric or venereal infection through a gram negative rod or chlamydia. Lover's heel is characteristic. Explosive arthritis (peripheral), urethritis, conjunctivitis. In AIDs patients, can develop keratodermia blenorrhagicum, which is hyperkeratosis on the hands and feet.
Rheumatoid Arthritis
Erosion and destruction of joints via inflammation. Associated with MHC Class II and a shared epitope motif. NEVER affects the DIP joints. TNF and IL-1 antibodies can improve symptoms. Susceptibility is by alleles of both DR1 and DR4.
RSV (Respiratory Syncytial Virus)
Idea here is that viral infection at the time of allergen exposure can predispose patients to developing allergies or conditions like asthma. RSV causes respiratory tract infections in patients of all ages. It is the major cause of lower respiratory tract infection during infancy and childhood. Recurrent wheezing and asthma are more common among individuals who suffered severe RSV infection during the first few months of life than among controls; whether RSV infection sets up a process that leads to recurrent wheezing or whether those already predisposed to asthma are more likely to become severely ill with RSV is a matter of considerable debate.
Describe 4 types of SCID.
(1)X-linked, usually occurs in young boys. Mutation of the common γ chain in cytokine signaling. Normal numbers of cells. (2) Autosomall recessive form of SCID is a JAK3 mutation which normally associates with the γ chain. Normal cell numbers. (3) Adenosine deaminase/Purine phosphorylase deficiency, impt. for purine metabolism, w/o it you get toxic metabolite buildup leading to lymphocyte death. (4)Bare Lymphocyte Syndrome: No MHC II so no CD4+ T cells caused by mutations in the MHC promoter transcription factors. MHC I disease results from a TAP1/2 mutation.
Sjogren's Syndrome
Associated with Rheumatoid Arthritis. Characterized by parotid and lacrimal gland inflammation, resulting in dry mouth and conjunctivitis.
Inflammation of the sacro-iliac joint. Lose the synovial capsule. Then T cells invade and form granulation tissue. The iliac side cartilage is eroded and the fibrotic ankylosis is ultimately replaced by bone, obliterating the SI joint entirely. Occurs in ankylosing spondylitis.
SLE (Systemic Lupus Erythematosis)
Type III hypersensitivity mechanism in which FcγReceptors are activated on Mast Cells, causing degranulation. Also activate NK cells. Immune complexes are deposited causing glomerulonephritis and vasculitis. Associated with MHC Class II. Patients produce auto-Abs to a number of self components. It is a B cell disease also, because auto-Abs mediate tissue destruction. Anti-Smith Ab is specific for SLE. Anti-Ro and Anti-La in fetal Lupus, which causes heart involvement. Antibodies also to dsDNA (ANA = anti nuclear Abs). Also Abs to phospholipids needed for clotting result in prlonged clotting test, although SLE patients are prothrombotic. Polyclonal hypergammaglobulinemia because B cells are secreting anti-self Abs. Splenomegaly, lymphopenia, thrombocytopenia, hemolytic anemia, fever, malaise, and weight loss. ANA test and Smith test via ELISA. Complement (C1q) deficiency in some of these patients. They are susceptible to encapsulated bacteria.
Vertebral disk inflammation. T cells invade the annulus and vertebral body, forming granulation tissue with activated MFs and fibroblasts. Annular fibers are replaced by fibrocartilage which ossifies and forms a syndesmophyte (bony stuff attached to a ligament). New bone formation changes the disk from an hourglass shape to a SQUARE. Bamboo spine, followed by osteoporosis.
MHC I associated autoimmune diseases. Activated CD8+ cells attack self-peptides. Affect more than simply the joints - eyes, skin, and mucous membranes are involved. Ankylosis = new bone formation. Susceptibility via HLA-B27 allele. There is deep, diffuse, dull low back or buttocks pain, due to cytokines and T cells eating away at the cartilage. The pattern of pain does not follow any nerve distribution. Pain is worst in the morning, better at night. Improves with exercise. No auto-Abs, immune complexes, or complement activation.
Sympathetic Ophthalmia
Injury to eye releases eye Ags into the bloodstream, which causes T cells to begin attacking the eye. Sympathetic ophthalmia (SO) is a granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It is the most dreaded complication of unilateral severe eye injury, as it can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury. Sympathetic ophthalmia is currently thought to be an autoimmune inflammatory response toward ocular antigens, specifically a delayed hypersensitivity to melanin-containing structures from the outer segments of the photoreceptor layer of the retina. The immune system, which normally is not exposed to ocular antigens, is introduced to the contents of the eye following traumatic injury. Once exposed, it senses these antigens as foreign, and begins attacking them. The onset of this process can be from days to years after the inciting traumatic event.
What is the immune response to Tetanus Toxin?
B cells with the appropriate Ig bind tetanus toxin and internalize it. They display the toxin on MHC II. CD4+ T cells bind to MHC II-peptide complex and are activated, stimulating the original B cells to secrete antibodies against the toxin into the blood. These Abs bind the toxin. This is why you need to be immunized against tetanus! Without the vaccine, the toxin can cause a lot of trouble.
Toxic Shock Syndrome (TSS)
TSS is caused by superantigens made by gram positive bacteria. These superantigens activate ALL T cells, regardless of their TCR specificity. High CD4+ activation. Must eliminate the source of the toxin and not use immunosuppression.
Graft Rejection
MHC molecules are the primary reason for graft rejection. A graft is only compatible if it is a match for all HLA alleles, meaning a two haplotype match at each loci for all alleles. Parents differ by one haplotype from their children. Siblings can be total matches.
PPD (Tuberculin Skin Test)
Mycobacterium TB exposure = primary infection. Inject PPD subcutaneously. DC will phagocytize the antigen and present it on MHC Class II to T cells. It will traffic to the lymph node to present to TH1 cells. If the body has been exposed to TB, there will be TH1 cells that recognize the antigen, and these TH1 cells will traffic to the infection site and cause inflammation by secreting cytokines such as IFN-gamma and IL-2, activating MFs and causing additional T cell proliferation and TH1 differentiation. Activated MFs make TNF and IL-1 which activate selectins. Previous infection causes a focus on inflammation at the site of inoculation.
Ulcerative Colitis
A form of inflammatory bowel disease. Has a superficial effect on the colon. There is an increase in IgG1. Bloody diarrhea. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Surgical removal of the large bowel is helpful.
Type I Allergic Rxn. Hives. Itchy red raised skin welts. Often have a pale border. The skin lesions of urticarial disease is caused by an inflammatory reaction in the skin, causing leakage from capillaries in the epidermis, resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells.The skin lesions of urticarial disease is caused by an inflammatory reaction in the skin, causing leakage from capillaries in the epidermis, resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells. Urticarial disease are thought to be caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin. This process can be the result of an allergic or non-allergic reaction, differing in eliciting mechanism of histamine release. In allergic urticaria, histamine and other pro-inflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high affinity cell surface receptors. Basophils and other inflammatory cells are also seen to release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases.
Wound Repair: what happens following epithelial injury?
MFs and DCs become activated and release cytokines and other chemokines recruiting other inflammatory cells to the site of infection. Chemokines attract the DC to lymphoid tissue (CCR7) so it can present the antigen to T cells. The pathogen determines whether the T cell response is primarily TH1 or TH2.
X-Linked Agammaglobulinemia
No B cells or Ig because of a mutation of Btk which signals from the pre-BCR to transition from heavy chain to light chain rearrangement. Never get past heavy chain rearrangement. T cells are completely fine.
X-linked Lymphoproliferative Disease
Can be caused in children with EBV with a mutation in T-cell development triggers (ZAP-70, lck, slam, slip)

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