IMMUNOLOGY Flashcards
(42 cards)
HLA associated with diseases:
HLA-A3
Hemochromatosis
HLA associated with diseases:
HLA-B27
PAIR
- Psoriasis
- Ankylosing spondylitis
- Inflammatory bowel disease
- Reactive arthritis (Reiter’s)
HLA associated with diseases:
HLA-DR3
DM1
HLA associated with diseases:
HLA-DR4
Rheumatoid arthritis
DM1
Follicular Dendritic cells
- not from bone marrow
- No MHC II and not APC
- only in lymph follicle
- help mature B cells
Characteristic finding on electron microscopy of a dendritic cell with Langerhans cell histiocytosis
- Birbeck granules (Tennis rackets), immature dendritic cells from monocyte lineage;
- do not stimulate T lymphocytes via antigen presentation.
- Express S-100 and CD1a
Site of negative selection for T-lymphocytes
- Corticomedullary junction of the thymus
- T-cells expressing TCR’s with high affinity for self undergo apoptosis
- Cells become either CD4 or CD8 T-cells
IL-12
- Induces helper T cell to become Th1 cell
- Virally infected cells secrete IL-12.
- More Th1 secrete IL-2 which stimulates cytotoxic T cells to kill virally infected cells
- IL-2 is the most important cytokine in activating antigen primed helper T cells
How do interferons work?
- induce production of ribonucleus that degrades viral mRNA (alpha and beta)
- Increase expression of MHC I and MCH II (gamma interferon) and antigen presentation
- Activate NK cells to kill virally infected cells
Macrophages of bone?
osteoclasts
gene complex RAG 1 and RAG 2
- gives rise to a protein that initiates VDJ recombination in B and T cell development
- Recognize Recombination Signal Sequences that flank VDJ sequences
- Rearrangement begins at breaks in the dsDNA located at the RSS
- Mutations in RAG genes lead to inability for VDJ recombination and arrest B and T cell development
When is passive immunity necessary?
To Be Healed Rapidly
- Tetanus toxoid
- Botulinum toxin
- HBV
- Rabies, (RSV for babies, once a month vaccine)
Screening for SLE?
Antinuclear antibodies (ANA)
nonspecific
Anti-dsDNA, anti-smith
More specific for SLE + Renal disease
Antihistone autoantibody
90% Drug induced lupus
Hydralazine
Seen in 50% of patients with SLE
Given the following features, what type of graft rejection is occuring?
Obliterative vascular damage
(Fibrosis of the graft tissue and blood vessels)
- Chronic rejection
- Months-years
- Class I MHCnon-self perceived by CTLs as class I MHCself presenting non-self antigens
- Irreversible
- T-cell and antibody mediated damage
Given the following features, what type of graft rejection is occuring?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate
- Acute rejection
- Weeks
- Cell mediated due to CTLs reacting against foreign MHCs
- Reversible with immunosuppresants
Given the following features, what type of graft rejection is occuring?
Macupapular rash, jaundice, diarrhea, hepatosplenomegaly
- GVHD
- Timeframe Varies
- Grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with “foreign” proteins resulting in severe organ dysfunction
- Usually occurs when organs rich in lymphocytes are donated: Bone and liver
Given the following features, what type of graft rejection is occuring?
Occlusion of graft vessels causing ischemia and necrosis
- Hyperacute rejection
- Within minutes!
- Antibody mediated (type II) due to presence of preformed anti-donor antibodies in transplant recipient
$ Types of Hypersensitivities
ACID
- Anphylactic and Atopic (type I) - free antigen cross links IgE on presensitized mas cells and basophils, releasing vasoactive amines acting on postcapillary venules.
- Cytotoxic (antibody mediated) (type II) - IgM, IgG bind and fix cell leading to lysis, recruit neutrophils and macrophages do most damage.
- Immune complex (type III) - Antigen-antibody (IgG) complexes activate complement, attracts neutorphils -> release lysosomal enzymes
- Delayed (cell mediated) (type IV) - Sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody)
4 T’s of Type IV hypersensitivity
- T lymphocytes
- Transplant rejections
- TB skin tests
- Touching ( contact dermatitis)
What causes more eosinophils in circulation?
DNAAACP + IL-5 (snot interleukin)
- Drugs
- Neoplastic
- Asthma , Atopic, Allergic processes, Churg strauss
- Addison’s
- Acute interstitial nephritis
- Collagen vascular diseases
- Parasites (invasive)
$$$ Bruton Agammaglobulinemia
- X-linked (Boys)
- B cell deficiency -> defective tyrosine kinase gene (BTK) -> low levels of all immunoglobulins
- Recurrent Bacterial infections after 6 months
- Absent thymic shadow
$$$ Thymic plasia (DiGeorge)
- 3rd and 4th pouches fail to develop
- No thymus -> No T cells
- No parathyroids -> low Ca2+ -> tetany
- Congenital defects in heart/great vessels
- Recurrent viral, fungal protozoal infections
- 90% have a chrom 22q11 deletion (detect with FISH)
- Absent thymic shadow on CXR