Chronic inflammation I Flashcards Preview

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Flashcards in Chronic inflammation I Deck (15):

What characterizes chronic inflammation?

a delayed but more specific response that is characterized by lymphocytes (buttons) and plasma cells (acentric nuclei with glassy cytoplasm) in tissue


Stimuli for chronic inflammation?

persistent infection, infection with virususes, mycobacteria, parasites, and fungi; autoimmune disease, foreign material, and some cancers


How does the T cell see antigen?

uses T cell receptor complex. TCR complex recognizes antigens presented on MHC
CD4 cells: use MHC class II; CD8 use MHC class I


How do you activate CD4 T cells?

1. binding of antigen/MHC complex
2. additional second signal
CD4 cell: occurs via exctracellular antigen that is phagocytosed, processed, and presented via MHC class II molecules on professional antigen presenting cells.
the second signal: B7 on APC binds CD28 on T cells. (28/7 =4)


What do CD4 T cells do once activated?

secrete cytokines that help inflammation.
can help B cells or CD8 T cells.


What are TH1 T cells?

CD4 t cells that help CD8 T cells.
does this via IL-2 and IFN-gamma
IL-2: T-cell growth factor and a CD8 T cell activator
IFN-g: macrophage activator


What do TH2 cells?

makes IL4 and IL5
IL4: causes class switching to IgG and IgE
IL-5: causes eosinophil chemotaxis and activation, maturation of B cells to plasmacells, and class switching to IgA
IL-10: inhibits the TH1 phenotype


How do you activate CD8 positive T cells?

intracellular antigen is processed and presented on MHC I
IL-2 from CD4 TH1 cells provides 2nd activation signal
cytotoxic T cells are then activated for killing.


How does cytotoxic killing occur?

secretion of perforins and granzyme; these induce apotosis of the target cell via caspase activation.
express Fas ligand. can bind Fas on target cell that activates apoptosis.


How do B cells start?

immature B cells made in the bone marrow and then undergo Ig rearrangement to become naive B cells that express surface IgM and IgD


How do B cells get activated?

1. antigen binds to surface IgM or IgD. then becomes a plasma cell and secrete IgM
2. B cell antigen presentation to CD4 helper cell via MHC II
CD40 receptor on B cell binds CD40 ligand on T cell: this provides the second signal for activation of the T cell.
activation of the T cell causes production of IL-4 and IL-5, which mediates B cell isotype switching, hypermutation, and maturation to plasma cells.


What is granulomatous inflammation?

subtype of chronic inflam
characterized by granuloma
key cell that defines a granuloma: epitheliod histiocyte (macrophages with abundant pink cytoplasm). granuloma = aggregation of epitheliod histiocyte
other common features: surrounded by giant cells and a rim of lymphocytes
these are divided into noncaseating and caseating subtypes


What are noncaseating graunlomas? What is the DDx of non-caseating granulomas?

they lack central necrosis
occur in as a rxn to foreign material, in sarcoidosis, beryllium exposure, crohn disease, and cat scratch disease. usually in the neck and gives a stellate granuloma. also see in Wegener's/granulomatosis with polyangiitis and Churg-Strauss, listeria


What is the DDx of caseating granuloma? what is a caseating granuloma? How do you distinguish btw different causes of caseating granulomas?

this is a granuloma with central necrosis
characteristic of TB and fungal infections
Do AFB stain to look for TB; do GMS stain to look for fungus


What are the steps involved in granuloma formation?

interaction btw macrophages and CD4 helper T cells. macrophages present antigen via MHC II to helper T cells.
then, macrophages secrete IL-12, which induces CD4 cells to differentiate into TH1 subtype. TH1 cells secrete IFN-gamma, which converts macrophages to epithelioid histiocytes and giant cells. (draw pic).
this happens for both caseating and non-caseating granulomas.

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