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Immune Hypersensitivities and Disorders (Hypersensitivity Reactions (Type…
Immune Hypersensitivities and Disorders
Hypersensitivity Reactions
Type 1
Immediate
IgE mediated
Special Fc part that attaches to mast cells
Allergic respone
Sensitization with 1st exposure
mucus mem switch to produce IgA (99%) or IgE (1%)
Second Exposure
Allergic Response
Must bind 2 IgE receptors together
Trigger mast cells to release histamines
Hives
Hayfever
Asthma
Anaphalaxis
Desensitization
Oral Immunotherapy of Ag
Anti AgE antibodies
To Fc part of IgE
rhuMab for asthma
Type 2 (Cytotoxivity)
Ab bind to hapten that bind to cells in body
NK cells bind to Fc part of Ab
Kill cell
Complement mediated lysis
E.g. Hemolytic disease of newborn
Rh mismatch
Mom Rh- and Dad Rh +
Rh foreign to mom but natural to dad
Moms B cell with produce Ab to destroy the RBC
Kills baby
Can prevent
Inject anti Rh Ab into Rh - mother
Soluble IgG compete with Moms B cells
Type 3 (immune complex disease)
Problem
Immune complexes that dont readily get phagoocytosed by macrophages
What type of immune complexes
small immune complex
made with too much Ab or Ag
Complement C3a recruited by these small immune complexes
Trigger complement fixation
Inflammation
C5a bring in neutrophils to area
Neutrophils kill cells instead of bacteria
Dead cells release DAMPS
create more inflammation and more dammage
tissue damage in organs
Type 4 (Cell mediated)
Only involve T helper and macrophage
1st time exposed
protein displayed APC MHC2
2nd time exposed
T helper find it and produce cytokines
Activate macrophages and makes them more hungry
Problem
usually occur in lymph nodes, but T helper cells can exsist in other places
Macrophages will come to part T cell originates from
Machrophage damage cells in the local region
E.g.
Poison Ivy
TB skin test
Prevention
Can be damped down with anti rejection drugs
Blocks T cell response
By looking at IL2
May hurt Immunocompromised people
Autoimmune Disease
reaction to self antigens
M gravis
Muscle cant contract
Antibody bind to acetocolyne receptor
T1 diabetes
T cyotoxic cell recog ilets used to make insulin
Rheumatoic arthritis
auto-Ag
collagen
Type 4 response
T helper cells recognize collagen in goingts
Type 3
B cells activated by T helper cytokines
Lupus
Auto-Ag
DNA
Can be from sunburn cause it release DNA
Anti-nuclear Ab
IgG for immune complex
Prevention
Take drugs that block B cell activation
Hygiene hypothesis
Explain increase autoimmune diseases
T reg cells
damp down auoimmune responses
may have decreased
Decreased native bacteria make less T reg cells
Gut bac produce CAMP
CAMP like short chain FA
Lead dendritic cells and gut macrohages to produce retanoic acid
T cells turned into T regulatory cells
Tolerance Response
On other hand
Inflammatory response would make dendritic cells into Tc cells
Treatment
Oral Immunotherapy
Stimulates IgA production
Out-compete allergen
Anti-IgE
Bind Fc part of IgE
Block binding to Mast cells
Probiotic therapy
replacing native flora
Usually all die in stomach from stomach acid
Prebiotic therapy
eat oligosaccarides
to feed bacteria already there in gut
larger exposure to good bacteria
Immunodeficiency Diseases
Primary
genetically inherited
failure to do VDJ joining
somatic recombination
cant produce B or T cells
Aquired
infection damage immune cells
HIV damage T cells
Def
Failure to produce one or more component of immune system