Flashcards in Immunology Deck (17):
In a parasitic infection, through what mechanism do eosinophils neutralize the infection?
In an allergic reaction, why is there an inflammatory response (having to do w/ eosinophils)?
Parasites: IL-5 is released by Th2 and mast cells, which activates and proliferates eosinophils. IgG and IgE antibodies then coat parasites and bind eosinophils degranulize and release cytotoxic material (ie Major Basic Protein) and kill parasites. This is Antibody-Dependent Cell-Mediated Cyotoxicity.
Allergic Reactions: Type 1 Hypersensitivity, release prostaglandins, cytokines, and leukotrienes which cause inflammation.
What do Th2 cells release to promote B-lymphocyte class switching for IgE synthesis? What do they release to activate eosinophils?
Th2 cells release IL-4 and IL-13 to promote B-lymph class switching.
They release IL-5 to activate eosinophils.
Which molecule (ie IL-?) is involved in pus formation?
Which cell type is present in caseating granulomas (as seen in TB), and what surface marker do they tend to have?
Large epithelial macrophages with pale pink granular cytoplasm. They have CD14 as their marker.
Side note. CD4 is for T-helper cells, CD8 is for T-killer cells.
What is the typical immune response to giardia?
Secretory IgA against giardia. Giardia tends to attack the duodenum and jejunum by binding to the intestine and then causing inflammation. If you are IgA deficient, you're more susceptible to Giardia.
Note: Eosinophils are NOT involved.
What cell type releases interferon gamma in response to m. tuberculosis?
A patient has defective signaling between CD4 and B cells. What type of immunoglobulin would be elevated, and what's it called?
IgM would be elevated b/c class switching of B lymphocytes would be off, making it more likely to have IgM.
Absense of CD40 ligand most common cause.
Remember, in class switching: the heavy chain constant region changes, the variable chain (giving antigenic variation) stays the same.
What are the important neutrophil chemotactic agents?
Leukotriene B4 (LTB4), 5-HETE, C5a (complement), IL-8
What is unique about IL-10?
It carries anti-inflammatory properties (particularly in inflammatory bowel disease).
IL-10 inhibits Th1 cytokines, MHII complex (and thus T helper cells), and suppresses macrophages and dendritic cells
What is the immunological response to toxoid vaccines?
Develop antitoxin antibodies (active immunity)
What are the 2 components of the MHC Class 1 proteins that the T cells recognize?
Heavy chain and beta 2 microglobulin
Which antibodies would be found in the following conditions?
Primary Biliary Cholangitis
Lupus-->Anti Double stranded DNA, anti-phospholipids
Rheumatoid Arthritis--> Anti Fc portion of IgG, anti-cirtullinated proteins
CREST syndrome-->Anti centromere
Infectious Mononucleosis-->heterophile antibodies (agglutinate sheep erythrocytes)
A patient has HIV-associated dementia. What is the likely finding on brain biopsy?
Groups of microglial cells form around areas of necrosis that then may form multinucleated giant cells.
What are the clinical findings in CREST syndrome? (Limited scleroderma)
*also look for fingertip ulcers
What are the 2 most common causes of SCID (Severe Combined Immuno Deficiency)?
1) X-linked SCID
2) Adenosine deaminase deficiency.
Adenosine is toxic to lymphocytes, so if it can't be eliminated it accumulates in lymphocytes and kills them. Thus, you need the try and either replace their blood (BMT) or somehow create adenosine deaminase (a retroviral vector to "infect" patients with it)
A young woman has arthralgias, a photosensitive skin rash, glomerulonephritis, and false positive Rapid plasma reagin (RPR) as well as a prolonged aPTT. What is the diagnosis, and what are they at risk of?
She likely has SLE with antiphospholipid antibodies (which we know because of prolonged aPTT and false positive RPR. It occurs in 30% of women with SLE).
They are at risk for venous and arterial thromboembolism as well as recurrent miscarriages.