Micro Lecture 25

Front 1

Type 1 HS (allergy)

Back 1

-IgE mediated
-sensitization with first exposure: IgA->IgE which attaches to mast cell
-second exposure leads to allergic reaction:allergin binds to multiple IgE on the mast cell at the same time (like T-independent)->mast cells release their granules which include histamine and prostaglandins

Front 2

IgE

Back 2

are created from IgM cells 1% of the time after first exposure and bind to mast cells, during the second exposure binds to allergin which causes the release of histamine and prostaglandins from mast cells like T-independent response

Front 3

Mast Cell

Back 3

are granules which release histamine and prostaglandins after antigens bind to the IgE receptors during second response which cause the allergic response

Front 4

Prostaglndin

Back 4

Are carried in mast cells and release during the second exposure when multiple IgE cells are bound to allergens

Front 5

Histamine

Back 5

Are carried in mast cells and release during the second exposure when multiple IgE cells are bound to allergens

Front 6

Leukotriene

Back 6

cause athsma when released with prostaglandins causing smooth muscle spasms=not treatable with antihistamines

Front 7

Sensitization

Back 7

induction of allergic responses

Front 8

Desensitization

Back 8

-injection of allergen into the blood stream in which we will mainly produce IgG because it is the serum antibody, enough IgG will bind to the allergin and neutralize it
-anti-IgE antibodies bind to the Fc part of IgE so it cannot bind to mast cells i.e rhuMab for athsma

Front 9

Anaphylaxis

Back 9

-like septic shock
-peanut allergy
-smooth muscle dilaters expand capillaries->diapedesis->hypovolemia->shock->death

Front 10

Hay Fever

Back 10

-mucus membranes in nasal passages

Front 11

Type 2 HS (cytotoxic)

Back 11

-not an allergic rxn because it involves NK cells
-antibody is mediated by complement or NK cells
-small molecule such as hapten is not recognized by our immune system until it binds to a cell and are introduced into the blood
-classic example is hemolytic disease of the newborn

Front 12

Hapten

Back 12

small molecule that is not recognized by our immune system until it binds to a cell

Front 13

ADCC

Back 13

NK bind to Fc part of an antigen whos Fab part is bound to a bacterium

Front 14

Hemolytic Disease of the Newborn

Back 14

-when mom is Rh- and dad is Rh+ so baby can be Rh+
-first born child's blood contacts the mother which elicits an immune response=ok
-second Rh+ child will elicit a secondary immune response in mom and lots of IgG produced against the babies red blood cells
-this is preventable by injecting anti-Rh antibodies during pregnancy and after each delivery: the IgG competes with Mom's B cells for the baby's blood and the mom is not sensitized i.e RhoGAM or Rhophyllac=essentially neutralizes the RBC

Front 15

RhoGAM

Back 15

example of anti-Rh antibodies which neutralize the baby's red blood cells because it prevents the binding of Mom's B cells to the baby's RBC's

Front 16

Type 3 HS (immune complex)

Back 16

-mediated by antibody and antigen agglutination into complexes
-the antigen is in excess so we get immune complexes that are small and cannot be phagocytosed well so it activates the complement system and recruits neutrophils (C5a) which release granules that will cause cell death around them which kills the cells that line our capillaries
-the tiny immune complexes get stuck in the basement membrane of our blood vessels which is worse than inflammation
-i.e rheumatoid arthritis and lupus

Front 17

Immune Complex

Back 17

-formed with agglutination of antibodies and antigen
-when antigen is in excess the immune complexes are small and are not phagocytosed well

Front 18

Antigen Excess

Back 18

-causes formation of small immune complexes which are not phagocytosed well
-complement system gets activated which recruit the neutrophils C5a and they release granules which cause cell death around them which kill the cells that line our capillaries and the tiny immune complexes get stuck in the basement membrane of our blood vessels which is worse than inflammation

Front 19

Basement Membrane

Back 19

-where the tiny immune complexes get stuck in our blood vessels which is worse than inflammation

Front 20

Neutrophil Degranulation

Back 20

-when the neutrophils (C5a) release granules which cause cell death around the cells that line our capillaries because of the excess of antigens

Front 21

Type 4 HS (delayed)

Back 21

-odd man out because its not mediated by antibodies
-mediated by Th cells and macrophages
-response peaks in days, not minutes
-sensitization with first exposure and Th cells become activated normally
-second exposure which happens a few days later: effector Th cells secrete cytokines and activate macrophages which cause inflammation
-i.e poison ivy, tissue rejection, nerve damage in leprosy, metal allergy, TB skin test

Front 22

Cell-mediated HS

Back 22

type 4 hypersensitivity

Front 23

Inflammation

Back 23

because of activation of macrophages from effector Th cells that secrete cytokines

Front 24

Anti-rejection Drugs

Back 24

cause patient to be immunocompromised
-cyclosporin:inhibits clonal expansion of T cells
-corticosteroids: reduce inflammation that causes tissue damage
-basiliximab: blocks IL-2 binding to T cells so prevents activation of T cells by Th cells

Front 25

Autoimmune disease

Back 25

-reactions to self antigens
-myasthenia gravis and Type 1 diabetes

Front 26

Myasthenia Gravis

Back 26

-B cells recognize ach receptors
-IgG neutralizes the AcH receptors and the AcH cannot bind to the muscle cell receptor and the muscles cannot contract
-ptosis is one symptom

Front 27

Type 1 diabetes

Back 27

-T cell receptors on T c cells recognize beta islet cells in the pancreas and the beta cells are destroyed which causes no production of insulin

Front 28

Rheumatoid Arthritis

Back 28

-Type 3 HS
-Th cells recognize collagen in joints which produce cytokines and cause inflammation (type 4 HS), activate B cells that may recognize collagen also and produce IgG against our collagen and immune complexes form

Front 29

Lupus

Back 29

-B cells recognize pieces of our own DNA
-IgG form immune complexes throughout the body, especially in capillaries
-butterfly rash
-benlysta blocks stimulatory B cell receptors to reduce B cell clonal expansion

Front 30

Hygiene Hypothesis

Back 30

-Relation of Treg cells, pathogen>native flora, and autoimmune problems
-too clean explains why we dont have native flora, too few T reg cells, increase in autoimmune disease
-bacteria in our gut is important and happens early
-leads to idea of treating autoimmune diseases by inducing oral tolerance which stimulates production of T reg cells and secrete IL-10

Front 31

Oral Tolerance

Back 31

treating autoimmune diseases by inducing oral tolerance which stimulates production of T reg cells and secrete IL-10

Front 32

Probiotic

Back 32

-try to eat good bacteria that contains bacteroides and clostridia to allow increased production of T reg cells

Front 33

Prebiotic

Back 33

-not proven useful in adults
-feed our native flora with oligosaccharides from breast milk

Front 34

Immunodeficiency Diseases

Back 34

failure to produce one or more components of the immune system

Front 35

Inherited IDD

Back 35

-SCID: stem cells dont do VDJ joining-no B or T cells
-Agammaglobulinemia: no B cells (x-linked disease)
-DiGeorge Syndrome: no thymus=no T cells
-Selective IgA deficiency: most common gentically inherited IDD

Front 36

Acquired IDD

Back 36

-measles: virus grows in T cells and weakens our cellular immunity
-multiple myeloma: B cell cancer, one B cell proliferates at the expense of the others
-HIV virus: slowly destroys Th cells