Homeostatic regulation of T lymphocytes is a central mechanism by which the immune system ensures its diversity and functionality. T cell deficiency triggers a proliferative response of T cells that remain within such conditions or that are adoptively transferred into such environments (which is often referred to as homeostatic proliferation or endogenous proliferation). The proliferation is often associated with a differentiation process that generates memory T cells. The resulting memory T cells are thought to play a critical role in the regulation of peripheral homeostasis as well as in the protection against invading pathogens.
There is substantial evidence suggesting that lymphopenia induced immune activation may result in autoimmunity, multiorgan immunopathology, as well as rejection of solid organ transplants. Therefore, understanding the mechanisms regulating T cell proliferation in lymphopenic conditions has fundamental biological importance. Our study aims at defining the mechanisms by which T cell proliferation/differentiation processes are induced and regulated.
Martin, B. N., T. Herjan, M. F. Gulen, K. Bulek, B. Min, and X. Li. (2016). T cell-intrinsic ASC critically promotes Th17-mediated experimental autoimmune encephalomyelitis. Nat. Immunol. In Press.
Do, J., A. Visperas, M. Freeman, E. Jang, S. Kim, B. Malissen, and B. Min. (2016). gd T cells support gut antigen reactive colitogenic effector T cell generation by enhancing antigen presentation by CD11b+ DCs in the mesenteric LN. Eur. J. Immunol. 46:340-346.
Do, J., A. Visperas, Y. O. Sanogo, J. J. Bechtel, N. Dvorina, S. Kim, E. Jang, S. A. Stohlman, B. Shen, R. L. Fairchild, W. M. Baldwin III, D. A. Vignali, and B. Min. (2016). An IL-27/LAG3 axis enhances Foxp3+ regulatory T cell suppressive function and therapeutic efficacy. Mucosal Immunol. 9:137-145.
Datta, S., N. Barrera, P. J. Pavicic, C. Zhao, M. Freeman, B. Min, and T. Hamilton. (2015). cEBP homologous protein expression in macrophages regulates the magnitude and duration of IL-6 expression and dextran sodium sulfate colitis. J. Interferon Cytokine Res. 35:785-794.
Do, J., W. M. Baldwin III, and B. Min. (2014). Spontaneous proliferation of H-2M-/- CD4 T cells results in unusual acute hepatocellular necrosis. PLoS One9(10): e110516. doi:10.1371.
Hwang, M., T. W. Phares, D. R. Hinton, S. A. Stohlman, C. C. Bergmann, and B. Min. (2015). Distinct effects of CD4 T cells on establishment of primary versus recall CD8 T cell responses during viral encephalomyelitis. Immunology144:374-386.
Visperas, A., J. Do, and B. Min. (2014). Cellular factors targeting APCs to modulate adaptive T cell immunity. J. Immunol. Res. 2014:750374. Epub 2014 Jul 14.
Visperas, A., B. Shen, and B. Min. (2014). gd T cells restrain extrathymic development of Foxp3+ inducible regulatory T cells via IFNg. Eur. J. Immunol. 44:2448-2456.
Do, J., K. Asosingh, W. M. Baldwin, and B. Min. (2014). Cutting Edge: IFNg signaling in non-T cell targets regulates T cell-mediated intestinal inflammation through multiple mechanisms. J. Immunol. 192:2537-2541.
Visperas, A., J. Do, K. Bulek, X. Li, and B. Min. (2014). IL-27, targeting antigen presenting cells, enhances Th17 differentiation and inflammation by upregulating Th17 promoting cytokine production. Mucosal Immunol.7:625-633.
Do, J., A. Visperas, M. L. Freeman, Y. Iwakura, M. Oukka, and B. Min. (2014). Colitogenic effector T cells: roles of gut homing integrin, gut antigen specificity and gd T cells. Immunol. Cell. Biol. 92:90-98.
Rao, K. N., C. Smuda, G. D. Gregory, B. Min, and M. A. Brown. (2013). Ikaros limits basophil development by suppressing C/EBPa expression. Blood122:2572-2581.
Do, J., A. Valujskikh, D. A. A. Vignali, R. L Fairchild, and B. Min. (2012). An unexpected role for MHCII-peptide complexes in shaping CD8 T cell expansion and differentiation in vivo. Proc. Natl. Acad. Sci. USA 109:12698-12703.
Zizhen, K., S. Swaidani, W. Yin, C. Wang, J. L. Barlow, M. F. Gulen, K. Bulek, J. Do, M. Aronica, A. N. McKenzie, B. Min, and X. Li. (2012). Epithelial cell-specific Act1 adaptor mediates IL-25-dependent helminth expulsion through expansion of Lin(-)c-Kit(+) innate cell population. Immunity 36:821-833.
Phares, T. W., S. A. Stohlman, M. Hwang, B. Min, D. R. Hinton, and C. C. Bergmann. (2012). CD4 T cells promote CD8 T cell immunity at the priming and effector site during viral encephalitis. J. Virol. 86:2416-2427.
Do, J., G. Foucras, A. F. Schenk, M. Shaw, G. Nunez, W. E. Paul, and B. Min. (2012). Both exogenous commensal and endogenous self antigens stimulate T cell proliferation under lymphopenic conditions. Cell. Immunol. 272:117-123.
Do, J., A. Visperas, R. L. O’brien, and B. Min. (2012). CD4 T cells enhance the generation of IL-17+ gd T cells. Immunol. Cell. Biol. 90:396-403.
Do, J., A. Visperas, K. Oh, S. A. Stohlman, and B. Min. (2012). Memory CD4 T cells induce selective expression of IL-27 in CD8+ DC and regulate homeostatic naïve T cell proliferation. J. Immunol. 188:230-237.
Do, J., A. Visperas, C. Dong, W. Baldwin, and B. Min. (2011). Cutting Edge: Generation of colitogenic Th17 CD4 T cells is enhanced by IL-17+ gd T cells. J. Immunol. 186:4546-4550.
Do, J., P.J. Fink, L. Li, R. Spolski, J. Robinson, W. J. Leonard, J. J. Letterio, and B. Min. (2010). Cutting Edge: Spontaneous development of IL-17-producing gd T cells in the thymus occurs via a TGFb1-dependent mechanism. J. Immunol. 184: 1675-1679.
Kim, S., M. Prout, H. Ramshaw, A. F. Lopez, G. Le Gros, and B. Min. (2010). Cutting Edge: Basophils are transiently recruited to the draining lymph node during helminth infection via IL-3 but infection-induced Th2 immunity develops without basophil LN recruitment or IL-3. J. Immunol. 184: 1143-1147.
Do, J. and B. Min. (2009). Differential requirements of MHC and of DCs for endogenous proliferation of different T-cell subsets in vivo. Proc. Natl. Acad. Sci. USA 106: 20394-20398.
Do, J. and B. Min. (2009). IL-15 produced and trans-presented by DCs underlies homeostatic competition between CD8 and gd T cells in vivo. Blood 113: 6361-6371.
Kim, S., T. Shen, and B. Min. (2009). Basophils can directly present or cross-present Ag to CD8 lymphocytes and alter CD8 T cell differentiation into IL-10-producing phenotypes. J. Immunol. 183: 3033-3039.