Date of Award


Degree Type


Degree Name

Master of Science


Microbiology and Immunology


Dr. Joaquin Madrenas

Second Advisor

Dr. Peter Blake

Third Advisor

Dr. Caigen Du


Two previous reports that RIP2 knockout (RIP2) mice had defective NF-κB signaling and Thl immune responses had led to the belief that this putative serinethreonine kinase might be a possible target for transplant immunosuppression. Thus, we tested whether RIP2 mice were able to reject vascularized allografts. Surprisingly, we found that T cells from RIP2= mice proliferated and produced IFNγ after allostimulation in vitro. Moreover, naïve RIP2/ CD4+ T cells differentiated normally into Thl or Th2 cells under appropriate cytokine microenvironments. Consistent with these findings, no difference in allograft survival was observed between wild type and RIP27 recipient mice, and rejection had similar pathology and cytokine profiles in both types of recipients. RIP2 deficiency was associated with defective NOD signaling but this did not affect TCR-dependent activation of the canonical NF-κB signaling or expression ofNF-κB genes in rejecting allografts. Our data demonstrate that RIP2-deficient mice have intact canonical NF-κB signaling, and can mount Thl-mediated alloresponses and reject vascularized allografts as efficiently as wild type mice, thus arguing against RIP2 as a primary target for immunosuppression.



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