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103 Cards in this Set

  • Front
  • Back
Antibodies for RA?
anti-IgG (rheumatoid factor)
Antibodies for SLE?
ANA, dsDNA, Smith
Antibodies for scleroderma?
centromere- CREST
Scl-70- diffuse
Anti-Jo?
polymyositis, dermatomyositis
Anti-Ro, Anti-La
Sjogren's
Anti-U1 RNP
mixed connective tissue disease
Anti-glutamate decarboxylase
Type 1 DM
Hormones that signal through a steroid receptor
Glucocorticoids, estrogen, progesterone, testosterone, aldosterone, vitamin D, T3/T4

- adrenal cortex hormones + vit D + T3/T4
Hormones that signal through a tyrosine kinase
Insulin, IGF-1, FGF, PDGF, Prolactin, GH
Hormones that signal through IP3
GnRH
GHRH
Oxytocin
ADH
TRH

"GGOAT"
Hormones that signal through cGMP
ANP, NO (vasodilators)
Hormones that signal through cAMP?
FSH, LH, ACTH, TSH, CRH
hCG
ADH
MSH
PTH
Calcitonin
Glucagon
Cells in medullary cords in lymph node
lymphs, plasma cells
cells in medullary sinuses in lymph node
reticular cells, macrophages- communicates with lymph
Paracortex not well developed
DiGeorge syndrome

- where T an B cells enter form blood
lymph node drainage from sigmoid colon
colic --> Inferior mesentery
lymph node drainage from rectum (above pectinate line)
Internal iliac
Anal canal below pectinate line - lymph drainage
superficial inguinal
Testes- lymph node drainage
para-aortic
Lateral side of the dorsum of the foot lymph node drainage
popliteal
Spleen- where are the t cells?
red pulp, periarterial lymphatic sheath (PALS)
spleen- where are the B cells?
white pulp- follicle
signs of post splenectomy
1. Howell-Jolly bodies (nuclear remnants)
2. Target cells
3. Thrombocytosis
which cytokine blocks Th1 maturation?
Il- 10 (produced by Th2)
Which cytokine blocks Th2 development
IFN-gamma (produced by Th1)
IgE
- stimulated by IL4
- binds mast cells (type1)
- helminths - eosinophil activation
IgA
- stimulated by IL5
- Secretions
- monomer in circulation, dimer when secreted
- Does not fix complement --> prevents attachment of bacteria and viruses to mucous membranes
loading of MHCI
RER- intracellular peptides
- viral immunity
- pairs with beta2-microglobulin- transport to cell surface
loading of MHCII
- APCs
- invariant chain leaves in acidified endosome
- alpha and beta chains of MHCII
HLA A3
hemochromatosis
HLA B27
Psoriasis
Ankylosing spondylitis
IBS
Reiter's syndrome
HLA B8
Graves' disease
HLA DR2
MS
hay fever
SLE
Goodpasture's
HLA DR3
DM1
HLA DR4
RA
DM1
HLA DR5
Pernicious anemia
Hashimoto's thyroiditis
HLA DR7
nephrotic syndrome- steroid responsive
NK cells enhanced by which cytokines
IL12
IFN-beta
IFN-alpha

*kills when no MHC I on cell
superantigen effect
cross link beta region of TCR to MHCII on APC --> IFNgamma from Th1 --> IL1, IL6, TNFalpha from macrophages
endotoxin receptor?
CD14 on macrophages

endotoxin = LPS
costim signal between Th cell and APC?
Th- CD28
APC- B7
signal 2 in Tc and MHCI interaction?
IL2 from Th cell activates Tc cell to kill virus infected cell
Signal 2 in B cell class switching?
B cell- CD40 receptor
Th- CD40 ligand
isotype
IgM, IgD etc
idiotype
antigen determines
antibodies that cross placenta?
IgG

NOT IgM
LPS on gram neg bacteria and polysaccharide capsular antigen- stimulate which part of immune response
1. macrophages via CD14
2. IgM antibodies but no immunologic memory
- not a peptide so cannot be presented on MHCI to T cells
- IgM is an antigen receptor on the surface of B cells
Deficiency of C5-C8 leads to susceptibility to which bug?
Neisseria
cytokine needed in differentiation of Th1
IFN gamma
Anaphlyaxis when exposed to blood products
Selective IgA deficiency
Cytokine with a function similar to GMCSF?
IL3
Cytokine: "Stimulates production of acute phase reactants and immunoglobulins."
IL-6
- secreted by Th and macrophages
IL8
- Secreted by macrophages
- Major chemotactic factor for neutrophils and C5a
IL-10
Secreted by Tregs
- Stimulates Th1, inhibits Th2
TNF
- Secreted by macrophages
- Mediates septic shock
- Causes leukocytie recruitment, vascular leak
CD16
Binds Fc and IgG
- NK cells
CD56
NK cells
Activation of classical complement pathway
IgG and IgM
Activation of alternative complement pathway
endotoxin or other molecules on the surface of microbes
C1-4
viral neutralization
C3b
opsonization, removal of immune complexes
C3a, C5a
Anaphylaxis
C5a
neutrophil chemotaxis
Classic and alternative pathways converge at...
C5
Cause of hereditary angioedema
Deficiency of C1 esterase inhibitor
- unregulated complement --> release of vasoactive substances
C3 deficiency
- severe, recurrent pyogenic sinus infections etc
- Increased Type III hypersensitivity- no clearing of immune complexes
DAF deficiency
GPI anchoring enzyme- cells can no longer anchor --> complement mediated lysis

- PNH of RBCs
Interferons in virus protection?
- inhibit viral protein synthesis by degrading viral mRNA
Bacteria that use antigen variation to evade immune system?
1. Salmonella - 2 flagellar variants
2. Borrelia - relapsing fever (except in lyme disease)
3. Neisseria gonorrhoeae- pilus protein
Parasites that use antigenic variation?
Trypanosomes
Granulomatous diseases
1. TB
2. Fungal (histo etc)
3. Syphilis
4. Leprosy
5. Cat scratch fever
6. Sarcoidosis
7. Crohn's disease
8. Berylliosis
Arthus reaction
Type III hypersensitivity
- Intradermal injection --> induces antibodies --> complex
- preformed antibodies circulation
- Seen 4-12 hours after a tetanus or diptheria vaccine

Test: immunofluorescent staining
Serum sickness
- Type III hypersensitivity
- 5-10 days after antigen exposure
- Mostly caused by drugs
- antibodies produced --> complex and deposit in membranes --> fix complement --> tissue damage
TB skin test- which kind of hypersensitivity?
Type IV- delayed
- T lymphs that have seen antigen bgefore release cytokines --> macrophage activation

NO ANTIBODY INVOLVED
characteristic of the Type II hypersensitivity diseases
- Specific to tissue where antigen is found

eg. hemoltyic anemia, pernicious anemia, ITP, erthyroblastosis fetalis, transfusion reactions, rheumatic fever, goodpasture's, bullous pemphigoid, pemphigus vulgaris, graves' disease, myasthenia gravis
Characteristic of Type III hypersensitivity diseases
Associated with vasculitis, systemic manifestaions

eg. SLE, RA, Polyarteritis nodosa, poststrep GN, serum sickness, arthus reaction, hypersensitivity pneumonities
MS- type of hypersensitivity?
IV
Guillan-Barre syndrome- type of hypersensitivity?
IV
Hashimoto's thyroiditis- type of hypersensitivity?
IV- some antibodies to TPO etc present but also cell mediated
Bruton's agammaglobuinemia
X-linked recessive
Defect in BTK (tyrosine kinase --> blocks B cell differentiation and maturation

Presents: recurrent bacterial infections after 6 months, no opsonization
Mutation in hyper IgM syndrome?
- CD40L on Th --> no class switching

Presents: severe pyogenic infections early in life
IgA deficiency
anaphylaxis on exposure to blood product with IgA
- hyper IgE --> rashes, itching etc
Common variable immunodeficiency
Decreased plasma cells, normal number of B cells
- defect in B cell maturation
Tetany, recurrent infections, congenital heart and great vessel defects
DiGeorge syndrome
- 22q11
- failure of 3rd and 4th arch development
- no thymus or parathyroids
retained primary teeth
Hyper IgE (Job's syndrome)
- No IFNgamma from Th cells --> no neutrophils recruited

Signs: course facies, cold staph abscesses, retained primary teeth, Increased IgE, derm- eczema

FATED
Causes of SCID
1. Defective IL-2 receptor - X linked
2. adenosine deaminiase deficiency- increase adenine--> toxic to B and T cells
3. Failure to synthesize MHC II antigens

- both B and T cells deficient

Tx: bone marrow transplant
Ataxia telangiectasia- immune problem?
- defect in DNA repair

Cerebellar defects, spider angiomas, IgA DEFICIENCY
Wiskott-Aldrich syndrome
WASP mutation, X linked
- Progressive deletion of B and T cells

TIE:
Thromboctyopenic purpura, Infections, Eczema

Low IgM, increased IgE, IgA
Leukocyte adhesion deficiency (LAD)
- LFA-1 integrin (CD18) defect on phagocytes
- autosomal recessive
- neutrophils cannot get to tissues or cannot phagocytose once they are there

signs: infections, no pus, delayed separation of umbilicus

Neutrophilia- unable to leave blood vessels to stuck in blood
Chediak-Higashi
- Decreased phagocytosis- defect in microtubular function
- autosomal recessive

signs: recurrent staph and strep with fever, PARTIAL ALBINISM, peripheral neuropathy
CGD
- lack of NADPH oxidase --> decreased ROS --> no respiratory burst in neutrophils

- Increased susceptibility to catalase positive organisms

test: negative Nitroblue tetrazolium dye reduction test
acute transplant rejection
weeks after transplant
- Tc against foreign MHC

tx: cylcosporine, OKT3
chronic rejection
Tcell and antibody
- vascular damage
- irreversible
- sees MHC presenting non self when it is really non self MHC

- months - years after transplant
GVHD
- graft T cells attack donor
Four immunosuprression drugs that lead to effects of decreased IL2?
1. cyclosporin- inhibits calcineurin, nephrotoxic
2. Tacrolimus- binds FK-binding protein- inhbits IL2 secretion, nephrotoxic
3. Sirolimus (rapamycin)- mTOR inhibitor- no T cell proliferation with IL-2 stimulation. NOT NEPHROTOXIC
4. Daclizumab- antibody against IL-2 recepton on T cells
Azathioprine
- converted to 6MP in body
- DNA synthesis inhibitor --> toxic to proliferating lymphs

6MP metabolized by xanthine oxidase --> do not use allopurinol

SE: bone marrow suppression
muromonab-CD3 (OKT3)
- binds CD3 on T cells --> blocking T cell signal transduction
mycophenolate mofetil
- block de novo guanine synthesis--> blocks lymphocyte production
Aldesleukin
IL2
used in renal cell carcinoma, metastatic melanoma
Oprelvekin
IL11

Used for thrombocytopenia
Rheumatoid factor
IgM Antibody against Fc portion of IgG
Anti desmin antibodies?
Crohn's disease
Antibodies to SS-A ribonucleoprotein
Sjogren's