Chronic inflammation I Flashcards Preview

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Flashcards in Chronic inflammation I Deck (15):
1

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

2

Stimuli for chronic inflammation?

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

3

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

4

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)

5

What do CD4 T cells do once activated?

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

6

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

7

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

8

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.

9

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.

10

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

11

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.

12

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

13

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

14

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

15

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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