Poison ivy

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 T_H1 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; T_H1 effector cell recognizes antigen

  • there must have been a prior exposure for there to be T_H1 effector cells around

• T_H1 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 T_H1 cells

• some of this antigen drifts up into lymph nodes and T_H1 cells get turned on

• if you are a severe T_H2 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 T_H1 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