Louis J. Picker

Some T cells are the immune system's memory chips. Before the immune system can mount an effective attack on a disease-causing microorganism, they must form a subset of "memory" T cells specific for that organism. These "memory" T cells orchestrate immune elimination of the invader and remain in the blood and tissues so that the system can mount another counterattack should the foreign agent invade again. Memory T cell activity is also the key to explaining how vaccines work. Vaccines expose the immune system to weakened or noninfectious forms of pathogens, thus activating T cell memory and tricking the system into generating these critical disease-fighting cells.

Researchers in Louis Picker's laboratory focus their studies on memory T cell biology in human and nonhuman primates. They investigate the physiology of T cell memory and effector responses, including mechanisms that control "selection" of the memory repertoire, the functional specialization of the memory population, and the elements involved in T cell homeostasis and regeneration.

At the same time, these scientists are seeking to determine the basis of effective immunity to certain chronic human pathogens, particularly HIV/SIV and cytomegalovirus, and are working on prophylactic and/or therapeutic vaccines against these pathogens. Finally, they are studying how memory T cells are reconstituted after HIV-1 infection or bone marrow transplantation.

Picker and his colleagues have developed special expertise in the quantification and functional characterization of antigen-specific memory T cells. They exploit these technologies in the examination of human subjects and rhesus macaque models of chronic viral infection.

Biography

Louis Picker graduated from UCLA with a B.S. in bacteriology in 1978 and took his M.D. degree at the University of California at San Francisco in 1982. After residency training in pathology at Beth Israel Hospital, Boston, and postdoctoral training in immunology at Stanford University Medical Center, he was appointed assistant professor and then associate professor of pathology at the University of Texas Southwestern Medical Center at Dallas. In 1999 he came to OHSU and ONPRC as professor of pathology/molecular microbiology and immunology in the OHSU School of Medicine and head of the Division of Pathobiology and Immunology.

Key Publications

Picker LJ, Reed-Inderbitzin EF, Hagen SI, Edgar JB, Hansen, SG, Legasse, A, Planer S, Piatak, Jr., M, Lifson, JD, Maino VC, Axthelm MK, and Villinger F. IL-15 induces CD4+ effector memory T cell production and tissue emigration in non-human primates. J. Clin. Invest.,116:1514-1524, 2006.

Okoye A, Meier-Schellersheim M, Brenchley JM, Hagen SI, Walker JM, Rohankhedkar M, Lum R, Edgar J, Planer SL, Legasse A, Sylwester AW, Piatak, Jr., M, Lifson, JD, Maino VC, Sodora DL, Douek DC, Axthelm MK, Grossman Z, and Picker LJ. Progressive CD4+ central memory T cell decline results in CD4+ effector memory insufficiency and overt disease in chronic SIV infection. J. Exp. Med., 204:2171-2185, 2007.

Price DA, Bitmansour AD, Walker JM, Edgar JB, Axthelm MK, Douek DC, and Picker LJ. Induction and evolution of cytomegalovirus-specific CD4+ T cell clonotypes in rhesus macaques. J. Immunol., 180:269-280, 2008.

Hansen SG, Vieville C, Whizin N, Coyne-Johnson L, Siess DC, Drummond DD, Legasse AW, Axthelm  MK, Oswald K, Trubey CM, Piatak, Jr. M, Lifson JD, Nelson JA, Jarvis  MA, and Picker LJ.  Effector-memory T cell responses are associated with protection of rhesus monkeys from mucosal SIV challenge. Nat. Med., 15(3):293-299, 2009.

Okoye A, Park H, Rohankhedkar M, Coyne-Johnson L, Walker JM, Planer SL, Legasse AW, Sylwester AW, Piatak, Jr. M, Lifson JD, Sodora DL, Axthelm MK, Schmitz JE, and Picker LJ.  Profound CD4+/CCR5+ T cell expansion is induced by CD8+ lymphocyte depletion but does not account for accelerated SIV pathogenesis.  J. Exp. Med., 206:1575-1588, 2009.

Hansen SG, Powers C, Richards R, Ventura AB, Ford JC, Siess D, Axthelm MK, Nelson JA, Jarvis MA, Picker LJ, Fruh K.  Evasion of CD8+ T cells is critical for super-infection by cytomegalovirus.  Science, 328:102-106, 2010.