 MHC1 works opposite from CD8+ T cells and NK

 Turn CD8 + T ON
 Turn NK OFF
 Therefore CD8 and NK don’t work at the same time
 any carpopedal spasm = HYPOCALCEMIA ( in child think missing parathyroid
glands)
 Wiskott- Aldrich : Eczema, recurrent infection, thrombocytopenia
-X-linked
-B and T cell deficiency
- WATER : W,A, thrombocytopenia purpura, eczema, recurrent infection
Lupus
 ANA( anti nuclear antibodies) : sensitive, not specific
 Anti-ds DNA is specific LUPUS
 AntiSMith/ snRNP’s is specific LUPUS
 Anti-phopholipid antibody
-cause (+) VDRL (False positive) AND prolonged PTT
-venous and arterial thromboemobilisim leading to fetal loss

 Delayed hypersensitivity is from the Th1 CD4+ T cells

 PUS is caused by neutrophils
-Attracted by IL-8, C5a, LT B4

Bradykinin -vasodilation + permeability

-smooth muscle contraction
- PAIN
Leukotriene C4 -vasoCONSTRICT + increase permeability
-bronchospasm

 Majority of myasthenia gravis patients have thymus abnormality ( thymoma,

thymic hyperplasia): appear as anterior mediastinal mass (in front of the veins)

 Guillain-Barre: CD 8+ T cells attack the endoneureium + cause demyelination PNS

 Polymyositis: symmetric proximal muscle weakness CD8+ mediated
- increase CK creatnine kinase
- increase anti-Jo1 antibodies
 Eosinophilic Myositis: eosiniophils infiltrate skeletal muscle (rare)
 Sarcoidosis high CD4: CD8 ratio! (negative PPD even if they are + bc all the cells
are sequestered at the lungs)
 Polymylagia rheumatic : bilateral stiffness in shoulder and pelvis. Fever,
weightloss, increase ESR. ASSOCIATED WITH TEMPORAL ARTERITIS

Transplants
  Hyper Acute: preformed antibodies. Occurs as soon as organ attached to vessels.
Thrombosis  ischemia and necrosis
-Type 2 hypersensitivity reaction
 Acute: vasculitis of the vessel
 Chronic: fibrosis of graft and blood vessel have smooth muscle proliferation so
obliterate
 Graft VS Host
 Bone marrow, liver transplant
 CD4 and 8 donor attack the recipient bc the MHC don’t match and
recognized as forgein
 Organs affected most : skin (desquamation), liver (jaundice), GI
(bleeding in poop)

 HIV
Gp120 binds to both CD4 + CCR5
Without CCR5 cant enter the cell ( a chemokine receptor )
-homozygous mutant = no infection with HIV
-heterozygous mutant = slow progression of disease
 CCR5 is on macrophages and dendritic cells ( reservoir)
 CxCR4 is on T cells
 Nef decrease expression MHC1
 Tat increase viral replication
Immunodeficiency
 X linked agammaglobinemia : Burton’s disease (only one where ONLY B CELLS ALL
MISSING AND NOTHING ELSE)
- tyrosine kinase not working
- B cells stop differentiating at Pre B cell
- Hypercellulairty in bone marrow with high PRE B CELL
- No immunoglobulins
 C3 deficiency : no MAC then Neisseria infections ( meningitides and gonorrhea)
 ATM ( Ataxia Telengiectasis Mutated)
-ATM gene
-cause DNA double stand breaks
-ataxia, teleangiectasis, and sinopulmonary infection (IgA deficiency)
 Chronic Granulomatous Disease: NADPH oxidase missing
-infection with CATALASE POSITIVE ( staph, pseudomonas, enteric like
E.coli, Klebsiella, Aspergillus)
- nitroblue tetrazolium test (-) if have it bc cant turn the test blue without
reactive oxygen species
- Catalase negative die bc the cells use H2O2 by myeloperoxidase to form
HOCL (hypochlorite/ bleach).
-Catalase + break down the H2O2 from its metabolisim.
 Hyper IgM: isotype switching now occurring ( alternative splicing) when the CD40
ligand on T cells is missing
 LAD Leukocyte adhesion deficiency: CD18 which is part of the integrin on leukocytes
is missing. Cant ENTER TISSUE
- HIGH WBC BLOOD
- No puss in inflammation or abcess
- Umbilical cord delayed separation
- Poor wound healing
- CD18 is beta chain of integrin
- Bacterial infection, viral normal

Random
 Cadherin: Calcium dependent adheres btw cells
 T cells with CD4 and CD8 on them are IMMATURE CORTICAL T CELLS (in cortex of
thymus (in medulla they have chosen either CD4 or 8 then) called DOUBLE
POSITIVE
 Tetanus toxin retrograde transport to CNS and prevents release of GABA and
glycine which are inhibitory transmitters
- Tetanus toxoid causes antibodies against the toxin
 Thymic epithelial cells have role in POSITIVE SELECTION
o Express MHC and see if they bind
o If mind then + select
o If don’t bind then apoptosis
 Eosinophils
1. Parasite : Antibody dependant Cytotoxicity : ADCC : IgE bind parasite and
then bind eosinophil to relase its granules
2. Type 1 hypersensitivity: release histaminase, to decrease histamine from
mast cell. Also LT to promote inflammation
 Eosinophils against ONLY HELMINTHS ( not giardia )
 Give RHOGam 28 weeks gestation and immediate post partum so that the IgG
will bind the Rh+ fetal cells before the mothers body can bind it and make
antibodies against it

Antiapoptosis Apoptosis
Bcl-2 Bcl-x ( L for live) = prevent Bak, Bax, Bim
cytochrome c existing mitochondria via
bax

CD15 = neutrophils and Reedsternburg cells in Hodgkins

IFN- alpha and beta cause synthesis antiviral proteins that degrade intracellular
mRna and impair protein synthesis
IL-10 and TGF- beta decrease inflammation