scispace - formally typeset
V

Vikas Saxena

Researcher at University of Maryland, Baltimore

Publications -  42
Citations -  534

Vikas Saxena is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Medicine & Immune system. The author has an hindex of 10, co-authored 23 publications receiving 311 citations. Previous affiliations of Vikas Saxena include Academia Sinica & Ohio State University.

Papers
More filters
Journal ArticleDOI

PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration

TL;DR: In this article , the authors show activated Tregs and CD4 effector T cells (Teffs) use PD-1/PD-L1 and CD80/PDL1, respectively, to regulate transendothelial migration across lymphatic endothelial cells (LECs).
Journal ArticleDOI

Lymph node fibroblastic reticular cells preserve a tolerogenic niche in allograft transplantation through laminin α4

TL;DR: Overall, FRC-Lama4 critically contributes to a tolerogenic LN niche by supporting T cell migration, constraining T cell activation and proliferation, and promoting Treg differentiation, and serves as a therapeutic target for immunoengineering.
Journal ArticleDOI

LTβR Signaling Controls Lymphatic Migration of Immune Cells.

Abstract: The pleiotropic functions of lymphotoxin (LT)β receptor (LTβR) signaling are linked to the control of secondary lymphoid organ development and structural maintenance, inflammatory or autoimmune disorders, and carcinogenesis Recently, LTβR signaling in endothelial cells has been revealed to regulate immune cell migration Signaling through LTβR is comprised of both the canonical and non-canonical-nuclear factor κB (NF-κB) pathways, which induce chemokines, cytokines, and cell adhesion molecules Here, we focus on the novel functions of LTβR signaling in lymphatic endothelial cells for migration of regulatory T cells (Tregs), and specific targeting of LTβR signaling for potential therapeutics in transplantation and cancer patient survival
Journal ArticleDOI

G-CSF promotes alloregulatory function of MDSCs through a c-Kit dependent mechanism.

TL;DR: In this article, G-CSF-induced myeloid-derived suppressor cells (MDSC) use a novel mechanism to suppress T cell responses, which may represent a therapeutic target for alloregulatory MDSCs.