Poison ivy

on 13.1.09 with 0 comments



Principles to understand

  • pentadecacatechol from the leaves makes covalent bonds with keratinocyte proteins, producing modified self that is analogous to viral infection

  • 2-3 days after a second exposure, T cells initiate delayed hypersensitivity reactions. they get there because of increased vascular permeability (due to scratches, say) and generalized inflammation. furthermore, scratching spreads the antigen

  • macrophages eat derivatized keratinocytes and this causes blisters

  • IgE is not involved

  • treatment is suppression of T cells locally or systemically


Type IV immune-mediated tissue damage

  • immune reactant is T cells

  • antigen can be soluble or cell-associated

  • if antigen is soluble, macrophages can ingest it, present it, and be activated by TH1 cells

  • if antigen is cell-associated, CD8+ T cells will effect a cytotoxic response (normally a virus-killing function)

  • examples: contact dermatitis, graft rejection

  • in graft rejection, the graft looks like modified self, just like it does in contact dermatitis

    • T cell looks at both the alpha helices of the MHC as well as the peptide sitting in groove

    • positive selection in thymus: T cell taught to recognize self MHC loosely, so there is a good chance it can recognize other MHC of the same species as well (10% of T cells recognize other non-self MHC)

    • but there is no negative selection for other MHCs, and no negative selection for problems of graft rejection (there is not enough time for evolutionary selection)

    • so if you have the ability to develop contact dermatitis (killing modified-self cells), you have the ability to reject grafts

  • rheumatoid arthritis, diabetes mellitus are also examples: combined T cell and antibody response (i.e., type III hypersensitivity responses)


Time course of contact dermatitis

  • swelling in skin can be as long as 2-3 days after exposure

  • antigen is injected; TH1 effector cell recognizes antigen

    • there must have been a prior exposure for there to be TH1 effector cells around

  • TH1 cells signal release of cytokines from macrophages

  • this can happen in the absence of any antibody

  • the long time course differentiates it from other types of responses



Antigen is processed by tissue macrophages and stimulates TH1 cells

  • some of this antigen drifts up into lymph nodes and TH1 cells get turned on

  • if you are a severe TH2 type person, you might not have a problem with poison ivy. however, you are probably more susceptible to viral infections

  • molecules involved are chemokines, cytokines, cytotoxins put out by TH1 cells: IFN-γ, TNF-α, chemokines, IL-3 (stimulates entire marrow), GM-CSF (stimulates a variety of hematopoietic cells, including monocytes and RBCs)


Category: Pathology Notes

POST COMMENT

0 comments:

Post a Comment