Immunology Week 4 Flashcards
Common allergies in children
milk, egg, peanut, wheat, soy, fish, shellfish
Common allergies in adults
peanut, nuts, shellfish, fish, fruits/veggies mild
What are the two types of food allergies and what are their typical symptoms?
IgE Mediated (urticaria, anaphylaxis), and non-IgE mediated (isolated GI reactions)
What goes wrong in the GI tract with allergy?
Food proteins usually stimulate a Treg response. In allergy, Th2 cells are generated directing IgE antibodies AND/OR T cells may produce cytokines causing eosinophilic reaction (IL5)
What happens in an IgE mediated allergy?
IgE specific for the food cross links, signals transduced, preformed mediators released (e.g., histamine). Clinical reactions ensue quickly
Oral Allergy Syndrome (pollen food syndrome)
Mouth itch usually with no Sx outside of mouth. Birch pollen usually associated with stone fruit allergy, ragweed with melon allergy.
Examples of non-IgE mediated allergies
enterocolitis, enteropathy, gastroenteritis, celiac. Eosinophilic esophagitis and atopic dermatitis in between.
Eosinophilic esophagitis
basically a rash of the esophagus. Furrows, rings, or white plaques on endoscopy
Anti-IgE
Binds only to Fc region of antibody
Desensitization vs. tolerance
tolerance long term and independent of other variables (basically cured).
EPIT
epicutaneus immunotherapy. Epithelial langerhans cells may induce regulatory and or Th-1 like responses with chronic exposure
What deficiencies lead to spontaneous tumors?
RAG-1 or RAG-2, perforin, IFNgamma, IL-12 or
B2-microglobulin
TILs
tumor infiltrating lymphocytes. Most often CD3
Do solid tumors express costimulatory molecules?
NO
Tumor Associated Antigens (TAA)
germline sequences normally silent, re-expressed embryonic antigens (not usually expressed, little tolerance), over expressed normal differentiation antigens, oncogenic viral antigens
Some non-mutated TAAs on human tumors?
cancer testis antigens, MUC1, Her2/neu, CEA, MART-1, tyrosinase, HPV, EBV, HBV and HCV
Some mutated TAAs on human tumors?
p53, p21ras,
Tumor cells are antigenic, so why don’t effector cells kill them?
peripheral tolerance (essentially autoimmunity), secretion of inhibitory cytokines (TGFbeta and IL10), tumor cells aren’t seen as different, Loss of MHC expression by tumors so can’t be recognized by T cells,
What happens to anti-tumor immunity as tumors increase?
It decreases
Passive immunotherapy
The infusion of antibodies or mature T cells to the patient to attack the tumor.
This type of therapy does not induce permanent change in the patient’s own immunity. NO MEMORY, short lived
Active immunotherapy
Tumor vaccines that directly stimulate the patient’s own immune cells to make a response against the tumor. Maybe long lived
ADCC
antibody dependent cellular cytotoxicity - tumor destruction induced through antibodies and NK cells or eosinophils
What are other ways antibodies can inhibit growth of cancer cells?
block receptors, deliver immunotoxins, or block checkpoint inhibitors (Prevents CTLA-4 or PD-1 engagement from inhibiting T cells)
CTLA-4
blocking it prevents down regulation of T cell proliferation, can’t bind B7
What is 5-FU?
cancer therapy drug
Why is RAG important?
For VDJ recombination.
Why is TAP important?
In the absence of TAP, peptides cannot enter the ER, so they are not loaded onto MHC class I molecules, also protecting the tumor cells from destruction by CD8+ cells.
How can carbohydrates be recognized as antigens?
By antibodies, not by T cells
How does X-linked agammaglobulinemia occur?
It occurs as a result of Bruton’s Tyrosine Kinase (BTK) deficiency. Don’t produce antibodies
How does Hyper IgM occur?
Hyper-IgM syndrome results from a CD40L deficiency, causing lack of class switching, memory and affinity maturation.
How does SCID occur?
There are many causes of SCID, which is a result of blocks in the maturation of both B and T cells.
What’s the most common immunoglobulin deficiency?
IgA
