Yuefeng Huang, Ph.D.
Assistant Professor of Microbiology & Immunology
Ph.D., Shanghai Institute of Biochemistry and Cell Biology
Innate lymphoid cells in infectious and inflammatory diseases
Higher-level organisms have evolved multi-layered immune systems, including physical barriers of skin and mucous membranes and soluble effector and cellular effector components to prevent pathologic colonization. Within these systems, adaptive T lymphocytes have for many years been considered the essential component of host cell-mediated immunity, using antigen-binding receptors to detect a wide array of ligands. In the past decade, another set of lymphocytes, namely innate lymphoid cells (ILCs), has been recognized to play critical roles in immunity against infections, especially during the early time window prior to T cell activation. ILCs lack antigen-specific receptors but resemble the effector phenotype and function of polarized T cell subsets in cytokine-induced cytokine production. ILC are enriched in mucosal barriers but are also found in secondary lymphoid or non-lymphoid tissues, contributing to host defense, tissue repair, metabolic homeostasis, inflammation and autoimmune disorders.
Our laboratory investigates the mechanism of ILC regulation and migration, ILC function in infectious and allergic diseases, ILC interaction with other immune or non-immune cells and how ILCs and microbiota regulate each another. Our goal is to develop a fundamental understanding of the biology of these recently characterized immune components so that we can better understand the roles of ILCs in infectious and inflammatory diseases. One of the main directions in the lab is studying ILC biology in the context of parasitic helminth infection and allergic asthma.
Postdoctoral positions are available.
Nagashima, H., Mahlaköiv, T., Shih, H.Y., Davis, F.P., Meylan, F., Huang, Y., Harrison, O.J., Yao, C., Mikami, Y., Urban, J.F. Jr., Caron, K.M., Belkaid, Y., Kanno, Y., Artis, D. and O'Shea, J.J. (2019) Neuropeptide CGRP limits Group 2 innate lymphoid cell responses and constrains Type 2 inflammation. Immunity 51: 1-14.
Baptista, A.P., Gola, A., Huang, Y., Milanez-Almeida, P., Torabi-Parizi, P., Murphy, T.L., Murphy, K.M., Virginia, S., Shapiro, V.S., Gerner, M.Y. and Germain, R.N. (2019) Ebi2 drives asymmetric intranodal distribution of CD4+ T cells to promote effective adaptive immunity. Immunity 50: 1188-1201.
Germain, R.N.* and Huang, Y.* (2019) ILC2s — resident lymphocytes pre-adapted to a specific tissue or migratory effectors that adapt to where they move? Curr. Opin. Immunol. 56: 76-81. *Corresponding authors.
Huang, Y.*, Mao, K.* and Germain, R.N. (2018) Thinking differently about ILCs-Not just tissue resident and not just the same as CD4+ T-cell effectors. Immunol. Rev. 286: 160-171. *Corresponding authors
Huang, Y.*, Mao, K., Chen, X., Sun, M., Kawabe, T., Li, W., Usher, N., Zhu, J., Urban, J.F. Jr., Paul, W.E. and Germain, R.N.* (2018) S1P-dependent inter-organ trafficking of group 2 innate lymphoid cells supports host defense. Science 359: 114-119. *Corresponding authors
Mao, K., Baptist, A.P., Tamoutounour, S., Zhuang, L., Bouladoux, N., Martins, A.J., Huang, Y., Gerner, M.Y., Belkaid, Y. and Germain, R.N. (2018) Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism. Nature 554: 255-259.
Kawabe, T., Jankovic, D., Kawabe, S., Huang, Y., Lee, P.-H., Yamane, H., Zhu, J., Sher, A., Germain, R.N., and Paul, W.E. (2017) Memory-phenotype CD4+ T cells spontaneously generated under steady state conditions exert innate Th1-like effector function. Science Immunol. 2: eaam9304.
Taylor, S.*, Huang, Y.*, Mallett, G., Stathopoulou, C., Felizardo, T.C., Sun, M., Martin, E.L., Zhu, N., Woodward, E.L., Elias, M.S., Reynolds, N.J., Paul, W.E., Fowler, D.H. and Amarnath, S. (2017) PD1 regulates KLRG1+ group 2 innate lymphoid cells. J. Exp. Med. 214: 1663-1678. *Co-first authors
Huang, Y*, and Paul, W.E. (2016) Inflammatory type 2 innate lymphoid cells. Int. Immunol. 28:23-28. *Corresponding author.
Huang, Y., Guo, L., Qiu, J., Chen, X., Hu-Li, J., Siebenlist, U., Williamson, P.R., Urban, J.F. Jr. and Paul, W.E. (2015) IL-25-responsive, lineage-negative KLRG1-high cells are multipotential "inflammatory" type 2 innate lymphoid cells. Nat. Immunol. 16: 161-169.
Guo, L., Huang, Y., Chen, X., Hu-Li, J., Urban, J.F. Jr. and Paul, W.E. (2015) Innate immunological function of TH2 cells in vivo. Nature Immunol. 16: 1051-1059.
Zhou, Y., Ge, R., Wang, R., Liu, F., Huang, Y., Liu, H., Hao, Y., Zhou, Q. and Wang, C. (2015) UXT potentiates angiogenesis via attenuating Notch signaling. Development 142: 774-786.
Wei, B., Cui, Y., Huang, Y., Liu, H., Li, L., Li, M., Ruan, K.C., Zhou, Q. and Wang, C. (2015) Tom70 mediates Sendai virus-induced apoptosis on mitochondria. J. Virol. 89: 3804-3818.
Huang, Y., Liu, H., Li, S., Tang, Y., Wei, B., Yu, H. and Wang, C. (2014) MAVS-MKK7-JNK2 defines a novel apoptotic signaling pathway during viral infection. PLoS Pathog. 10:e1004020.
Huang, Y., Liu, H., Ge, R., Zhou, Y., Lou, X. and Wang, C. (2012) UXT-V1 facilitates the formation of MAVS antiviral signalosome on mitochondria. J. Immunol. 188: 358-366.
Huang, Y., Chen, L., Zhou, Y., Liu, H., Yang, J., Liu, Z. and Wang, C. (2011) UXT-V1 protects cells against TNF-induced apoptosis through modulating complex II formation. Mol. Biol. Cell22: 1389-1397.
Lou, X., Sun, S., Chen, W., Zhou, Y., Huang, Y., Liu, X., Shan, Y. and Wang, C. (2011) Negative feedback regulation of NF-kappaB action by CITED2 in the nucleus. J. Immunol. 186: 539-548.