Sentence examples for lymphocyte polarization from inspiring English sources

Indeed, we have previously shown that neutrophil-derived extracellular traps (NETs) can downregulate dendritic cell activation in vitro, thereby inducing Th2 T lymphocyte polarization [27].

By binding downstream effectors like regulator for cell adhesion and polarization enriched in lymphoid tissues (RAPL) and Rap1-GTP-interacting adaptor molecule (RIAM), Rap1 connects to talin [12] and induces lymphocyte polarization by distributing LFA-1 to the leading edge, which is indispensable for cellular adhesion and migration [13], [14].

Conversely, Th2 cells induced naïve B lymphocyte polarization into Be2 cells, which produced IL-4 and IL-6, in the unexpected absence of GATA-3.

In fact, M2 polarization is generally associated with Th2 lymphocyte polarization and with expression of pro-fibrogenic factors, such as TGF-β [ 31].

Furthermore, B lymphocyte polarization into type-1 B effector (Be1) and Be2 cells and B-cell modulating factors of the TNF family, most notably the B-cell-activating factor (BAFF), and their prominent role in SS are additional complicating factors.

In particular, several miRNAs have been shown to regulate pathways underlying AAD pathogenesis including T-lymphocyte polarization and function [ 7– 9], regulatory T-cell activity [ 10], and airway smooth muscle proliferation and contractility [ 11– 13].

Thus, for T lymphocytes, polarization and imprinting of inflammatory responses is regulated by dynamic interaction of IFN-γ and IL-12, and regulation of expression of the IL-12 receptor.

In recent years, it has been reported that UC-MSCs could meliorate clinical parameters and histology by improving kidney fibrosis and modulating the inflammatory response (including inhibiting lymphocytes, inducing polarization of Th2 cytokines, and inhibiting proinflammatory cytokines) in experimental lupus nephritis [ 27, 28].

Based on the function of the spleen as a site of antigen presentation, B- and T-lymphocyte activation, and polarization of cytokine responses, chronic stress induces morphological changes that might alter cellular and humoral immune responses.

Across several cancer types the extent of tumour infiltrating lymphocytes, and their polarization toward cytotoxic T/natural killer (NK) cell gene expression linked to an IFNγ-STAT1-IRF1 signaxisng axis has been identified as a feature associated with good prognosis [ 4].

Subsequent studies looking at the mechanisms showed that the treatment effect was not due to a direct engraftment and differentiation into renal tissue but rather to the inhibition of lymphocytes, the induced polarization of T helper 2 cytokines, and the inhibition of the synthesis of pro-inflammatory cytokines.