Nicholas Carpino

Associate Professor

Department of Microbiology and Immunology
Ph.D., Stony Brook University, 1997

(631) 632-4610
(631) 632-9797




Research in the Carpino Lab focuses broadly on host-pathogen interactions, the regulation of the mammalian immune response, and how intertwined biochemical regulatory mechanisms involving protein phosphorylation, protein ubiquitination, and lipid signaling control these inflammatory pathways.  We study aspects of both innate and adaptive immunity.  We are interested in understanding how the immune system balances the conflicting needs of eliminating dangerous microbes without simultaneously harming the host. 

One current project focuses on the role of two homologous phosphatase enzymes, Sts-1 and Sts-2, in regulating host innate immune responses to infection by a variety of different human pathogens.  Interestingly, mice lacking Sts protein expression are profoundly resistant to systemic infection by the fungal pathogen Candida albicans and bacterial pathogens such as Staphylococcus aureus (Gram positive) and Francisella tularensis (Gram negative).  The Sts-/- phenotype is significant, because the resistance appears due to a more effective immune response, rather than a hyper-inflammatory reaction that results in collateral tissue damage.  From our studies on the effects of Sts deletion, we have learned that minor shifts in the threshold of activation of the immune response can have profound consequences on the outcome of a pathogen infection.

Another area of interest is how T cell signaling pathways control lymphocyte growth, development and function. Finally, another area of study involves understanding the regulation of a key T cell tyrosine kinase, Zap-70.  By further understanding immunoregulatory signaling mechanisms, we hope to contribute to the development of strategies that promote effective anti-microbial immune responses. This is particularly important an era when the development of antibiotic resistance by a number of micro-organisms is becoming a growing public health threat.