Regulation of FoxP3+ Regulatory T Cells and Th17 Cells by Retinoids

Vitamin A has both positive and negative regulatory functions in the immune system. While vitamin A is required for normal formation of immune cells and epithelial cell barriers, vitamin A deficiency can lead to increased inflammatory responses and tissue damage. The mechanism with which vitamin A and its metabolites such as retinoids negatively regulate inflammatory responses has not been clearly defined. Recently, it has been established that retinoids promote the generation of immune-suppressive FoxP3+ regulatory T cells while they suppress the T cell differentiation into inflammatory Th17 cells in the periphery such as intestine. These novel functions of retinoids provide a potentially important immune regulatory mechanism. In this review, we discuss the functions of retinoids in the development of the FoxP3+ cells and Th17 cells, the phenotype and functions of retinoid-induced FoxP3+ T cells, and the impact of retinoid-induced FoxP3+ T cells on the immune tolerance

Homeostatic and pathogenic extramedullary hematopoiesis

Extramedullary hematopoiesis (EH) is defined as hematopoiesis occurring in organs outside of the bone marrow; it occurs in diverse conditions, including fetal development, normal immune responses, and pathological circumstances. During fetal development, before formation of mature marrow, EH occurs in the yolk sac, fetal liver, and spleen. EH also occurs during active immune responses to pathogens. Most frequently, this response occurs in the spleen and liver for the production of antigen-presenting cells and phagocytes. EH also occurs when the marrow becomes inhabitable for stem and progenitor cells in certain pathological conditions, including myelofibrosis, where marrow cells are replaced with collagenous connective tissue fibers. Thus, EH occurs either actively or passively in response to diverse changes in the hematopoietic environment. This article reviews the key features and regulators of the major types of EH

Retinoic Acid Differentially Regulates the Migration of Innate Lymphoid Cell Subsets to the Gut

SummaryDistinct groups of innate lymphoid cells (ILCs) such as ILC1, ILC2, and ILC3 populate the intestine, but how these ILCs develop tissue tropism for this organ is unclear. We report that prior to migration to the intestine ILCs first undergo a “switch” in their expression of homing receptors from lymphoid to gut homing receptors. This process is regulated by mucosal dendritic cells and the gut-specific tissue factor retinoic acid (RA). This change in homing receptors is required for long-term population and effector function of ILCs in the intestine. Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent homing receptor switch in gut-associated lymphoid tissues. In contrast, ILC2 acquire gut homing receptors in a largely RA-independent manner during their development in the bone marrow and can migrate directly to the intestine. Thus, distinct programs regulate the migration of ILC subsets to the intestine for regulation of innate immunity

Estimating Form Factors of Bs→Ds(∗)B_s\rightarrow D_s^{(*)} and their Applications to Semi-leptonic and Non-leptonic Decays

$B_s^0\rightarrow D_s^{-}$ and $B_s^0\rightarrow D_s^{*-}$ weak transition form factors are estimated for the whole physical region with a method based on an instantaneous approximated Mandelstam formulation of transition matrix elements and the instantaneous Bethe-Salpeter equation. We apply the estimated form factors to branching ratios, CP asymmetries and polarization fractions of non-leptonic decays within the factorization approximation. And we study the non-factorizable effects and annihilation contributions with the perturbative QCD approach. The branching ratios of semi-leptonic $B_s^0\rightarrow D_s^{(*)-}l^+\nu_l$ decays are also evaluated. We show that the calculated decay rates agree well with the available experimental data. The longitudinal polarization fraction of $B_s\rightarrow D_s^*V(A)$ decays are $\sim0.8$ when $V(A)$ denotes a light meson, and are $\sim0.5$ when $V(A)$ denotes a $D_q$ ($q=d,s$) meson.Comment: Final version published in J Phys. G 39 (2012) 045002 (Title also changed