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7 Cards in this Set

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  • Back
Burkitt's Lymphoma (FAB L3)
Mistake in B-cell rearrangement. Immunoglobulin gene accidentally joined to gene involved in cellular growth. Results in B-cell tumors
X Linked Agammaglobulemia
sex linked. Bcell develpment stops at pre B cell stage. Recurrent EC infections:

Haemophilus influenzae
Streptococcus pneumoniae
Streptococcus pyogenes
Staphylococcus aureus
Patients must be treated with antibiotics and immunoglobulin from pooled blood
Mutiple Myeloma
Malignancy of plasma cells at the end stage of Bcell development
Causes bone disease-tumors arise in bone marrow=erosion of bone
Excess production of monoclonal antibody- IgG or IgA. Excess production of light chains that are excreted in urine. Bence Jones proteins occur upon heating the urine.
Increase sedimentation occurs-Rouleaux formation
T cells recognize
Processed proteins
The co-stimulatory receptor on an epithelial cell is ______.
CD4
CD28
CD80/CD86
CD3
none of these. no antigen presenting cell because its an epithelial cell. it only presents to a T cell.
Superantigens
Superantigens (SAgs) are a distinct class of antigens that stimulate a primary T cell response after being presented as an intact protein molecule (unlike as a peptide: MHC complex) by MHC class II molecules

Bacterial superantigens: Staphylococcal enterotoxin (SE), Toxic shock syndrome toxin (TSST)

Viral superantigen (yet to be established, antigen not characterized): Rabies viral antigen and Epstein Barr viral antigen

Superantigen binds to the Vb region of TCR and to the outer surface of MHC class II molecule.

SAg induces a polyclonal T cell response resulting in production of large amount of cytokines (IL-1, IL-2, TNF-a) responsible for inducing a systemic shock, hence Toxic shock syndrome.

SAg also inhibits induction of specific adaptive response which favors the pathogenicity of the bacteria.

Bacterial superantigens: Staphylococcal enterotoxin (SE), Toxic shock syndrome toxin (TSST)

Viral superantigen (yet to be established, antigen not characterized): Rabies viral antigen and Epstein Barr viral antigen

Superantigen binds to the Vb region of TCR and to the outer surface of MHC class II molecule.

SAg induces a polyclonal T cell response resulting in production of large amount of cytokines (IL-1, IL-2, TNF-a) responsible for inducing a systemic shock, hence Toxic shock syndrome.

SAg also inhibits induction of specific adaptive response which favors the pathogenicity of the bacteria.
Bacterial superantigens: Staphylococcal enterotoxin (SE), Toxic shock syndrome toxin (TSST)

Viral superantigen (yet to be established, antigen not characterized): Rabies viral antigen and Epstein Barr viral antigen

Superantigen binds to the Vb region of TCR and to the outer surface of MHC class II molecule.

SAg induces a polyclonal T cell response resulting in production of large amount of cytokines (IL-1, IL-2, TNF-a) responsible for inducing a systemic shock, hence Toxic shock syndrome.

SAg also inhibits induction of specific adaptive response which favors the pathogenicity of the bacteria
bare lymphocyte syndrome
Deficiency of TAP protein cause a rare disease called bare lymphocyte syndrome

• <1% MHC class I molecule expression

• Poor CD8 response

• Chronic viral respiratory infection