Tohoku University · Immunology and Microbiology
Professor Takeshi Kawabe's research lab focuses on the immunological mechanisms governing T cell homeostasis, particularly the development, differentiation, and functional heterogeneity of memory-phenotype (MP) CD4⁺ T cells. The lab investigates how homeostatic proliferation and cytokine signals—such as IL-7 and IL-12—drive the generation of innate-like effector functions in MP T cells, with a special emphasis on T-bet-high subsets involved in rapid immune responses. Their work also explores organ-specific T cell responses, especially in mucosal tissues like the gut, and the regulation of FcεR2/CD23 in immune cells. These studies contribute to understanding immune memory, autoimmunity, and allergic inflammation at the molecular and cellular levels.
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These results suggest that EPBD is a safe and effective technique for the treatment of common bile duct stones in patients with liver cirrhosis.
Conventional CD4<sup>+</sup> T cells are composed of naïve, pathogen-specific memory, and pathogen-independent memory-phenotype (MP) cells under steady state. Naïve and pathogen-specific memory cells play key roles in adaptive immunity, whereas the homeostatic mechanisms regulating the generation of MP cells and their biological functions are unclear. We show that MP cells are autonomously generated from peripheral naïve cells in the absence of infectious stimulation in a T cell receptor (TCR)-
The regulation of human low affinity FcR for IgE (Fc epsilon R2/CD23) and the soluble Fc epsilon R2 [IgE binding factor (BF)] of monocyte (U937), T (ED), and B (JIJOYE) cell lines was examined by anti-Fc epsilon R2 mAb (H107, Mab176) and the cDNA probe for Fc epsilon R2. The effect of IL-4 and IFN-gamma on Fc epsilon R2 regulation was variable among these three cell lines. IL-4 and IFN-gamma enhanced the Fc epsilon R2 gene expression and the production of Fc epsilon R2 and IgE-BF on U937, wherea
Homeostatic proliferation of naive T cells in the spleen and cutaneous lymph nodes supplies memory-phenotype T cells. The "systemic" proliferative responses divide distinctly into fast or slow cell division rates. The fast proliferation is critical for generation of effector memory T cells. Because effector memory T cells are abundant in the lamina propria of the intestinal tissue, "gut-specific" homeostatic proliferation of naive T cells may be important for generation of intestinal effector me
Conventional CD4<sup>+</sup> and CD8<sup>+</sup> T lymphocytes comprise a mixture of naive and memory cells. Generation and survival of these T-cell subsets is under strict homeostatic control and reflects contact with self-major histocompatibility complex (MHC) and certain cytokines. Naive T cells arise in the thymus via T-cell receptor (TCR)-dependent positive selection to self-peptide/MHC complexes and are then maintained in the periphery through self-MHC interaction plus stimulation via inte
CD4<sup>+</sup> T lymphocytes consist of naïve, antigen-specific memory, and memory-phenotype (MP) cell compartments at homeostasis. We recently showed that MP cells exert innate-like effector function during host defense, but whether MP CD4<sup>+</sup> T cells are functionally heterogeneous and, if so, what signals specify the differentiation of MP cell subpopulations under homeostatic conditions is still unclear. Here we characterize MP lymphocytes as consisting of T-bet<sup>high</sup>, T-bet<
T cells of the small intestine, including Th17 cells, are critically involved in host protection from microbial infection, and also contribute to the pathogenesis of small bowel inflammatory disorders. Accumulating evidence suggests that mesenteric lymph nodes (MLNs) play important roles in gut-tropic T-cell generation, although it is still unclear if MLNs are involved in the pathogenesis of small intestine inflammation. To address this issue, we analyzed the roles of both MLNs and Peyer's patch
In conventional adaptive immune responses, upon recognition of foreign antigens, naive CD4+ T lymphocytes are activated to differentiate into effector/memory cells. In addition, emerging evidence suggests that in the steady state, naive CD4+ T cells spontaneously proliferate in response to self-antigens to acquire a memory phenotype (MP) through homeostatic proliferation. This expansion is particularly profound in lymphopenic environments but also occurs in lymphoreplete, normal conditions. The
Under steady-state conditions, conventional CD4<sup>+</sup> T lymphocytes are classically divided into naïve (CD44<sup>lo</sup> CD62L<sup>hi</sup>) and memory (CD44<sup>hi</sup> CD62L<sup>lo</sup>) cell compartments. While the latter population is presumed to comprise a mixture of distinct subpopulations of explicit foreign antigen (Ag)-specific "authentic" memory and foreign Ag-independent memory-phenotype (MP) cells, phenotypic markers differentially expressed in these two cell types have yet
Abstract CD4+ T cells are composed of naïve, pathogen-specific memory, and pathogen-independent memory-phenotype (MP) cells. Naïve and pathogen-specific memory cells play key roles in adaptive immunity while the homeostatic mechanisms regulating the generation of MP cells and their biological functions are unclear. In this work we show that MP cells are autonomously generated from peripheral naïve cells in the absence of infectious stimulation in a TCR- and CD28-dependent manner. We further demo
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