scholarly journals Correction: Critical Role of p38 and GATA3 in Natural Helper Cell Function

2014 ◽  
Vol 193 (3) ◽  
pp. 1512-1512
Author(s):  
Jun-ichi Furusawa ◽  
Kazuyo Moro ◽  
Yasutaka Motomura ◽  
Kazuo Okamoto ◽  
Jinfang Zhu ◽  
...  
Keyword(s):  
Cell Function ◽  
Critical Role ◽  
Helper Cell ◽  
Natural Helper

scholarly journals Critical Role of p38 and GATA3 in Natural Helper Cell Function

2013 ◽  
Vol 191 (4) ◽  
pp. 1818-1826 ◽  
Author(s):  
Jun-ichi Furusawa ◽  
Kazuyo Moro ◽  
Yasutaka Motomura ◽  
Kazuo Okamoto ◽  
Jinfang Zhu ◽  
...  
Keyword(s):  
Cell Function ◽  
Critical Role ◽  
Helper Cell ◽  
Natural Helper

Critical role of c-Kit in beta cell function: increased insulin secretion and protection against diabetes in a mouse model

Diabetologia ◽  
2012 ◽  
Vol 55 (8) ◽  
pp. 2214-2225 ◽  
Author(s):  
Z. C. Feng ◽  
J. Li ◽  
B. A. Turco ◽  
M. Riopel ◽  
S. P. Yee ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Mouse Model ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Critical Role

scholarly journals The role of CD154 in organ transplant rejection and acceptance

2001 ◽  
Vol 356 (1409) ◽  
pp. 691-702 ◽  
Author(s):  
Allan D. Kirk ◽  
Patrick J. Blair ◽  
Douglas K. Tadaki ◽  
He Xu ◽  
David M. Harlan
Keyword(s):  
T Cell ◽  
Cell Function ◽  
Transplant Rejection ◽  
Critical Role ◽  
Organ Transplant ◽  
The Past ◽  
Costimulatory Signals ◽  
Intensive Investigation ◽  
Antigen Presenting

CD154 plays a critical role in determining the outcome of a transplanted organ. This simple statement is amply supported by experimental evidence demonstrating that anti–CD154 antibodies are potent inhibitors of allograft rejection in many rigorous transplant models. Unfortunately, despite intensive investigation over the past ten years, the precise mechanisms by which antibodies against CD154 exert their anti–rejection effects have remained less obvious. Though originally classified with reference to B–cell function, CD154–CD40 interactions have also been shown to be important in T cell–antigen–presenting cell interactions. Accordingly, CD154 has been classified as a T–cell co–stimulatory molecule. However, mounting data suggest that treatment with anti–CD154 antibodies does not simply block costimulatory signals, but rather that the antibodies appear to induce signalling in receptor–bearing T cells. Other data suggest that anti–CD154 effects may be mediated by endothelial cells and possibly even platelets. In fact, the current literature suggests that CD154 can either stimulate or attenuate an immune response, depending upon the model system under study. CD154 has secured a fundamental place in transplant biology and general immunology that will no doubt be the source of considerable investigation and therapeutic manipulation in the coming decade.

The Evolving Role of MicroRNAs in Endothelial Cell Dysfunction in Response to Infection

2018 ◽  
Vol 44 (03) ◽  
pp. 216-223 ◽  
Author(s):  
Rebecca Watkin ◽  
Glenn Fitzpatrick ◽  
Steve Kerrigan
Keyword(s):  
Endothelial Cell ◽  
Cardiovascular System ◽  
Noncoding Rna ◽  
Target Genes ◽  
Cell Function ◽  
Critical Role ◽  
Microbial Infection ◽  
Endothelial Cell Function ◽  
Rna Molecules

AbstractThe microRNAs are short noncoding RNA molecules responsible for translational repression and silencing of target genes via binding to the mRNA. They are found in all eukaryotic cells and play a critical role in virtually all physiological processes, including within the cardiovascular system where they influence cellular development, differentiation, cardiovascular function, hemostasis, and programmed cell death. Dysregulated microRNA expression is associated with several conditions ranging from cancer and autoimmune disease to infection. Progressively, it has become increasingly clear that microRNAs are important components of the host response to microbes. The cardiovascular system, coupled with cells of the innate immune system, provide the initial interaction and first response to microbial infection, respectively. This review presents the current state of knowledge regarding the role of microRNAs with emphasis on their role in controlling endothelial cell function.

scholarly journals IMMUNOLOGICAL TOLERANCE IN BONE MARROW-DERIVED LYMPHOCYTES

1974 ◽  
Vol 139 (6) ◽  
pp. 1464-1472 ◽  
Author(s):  
David H. Katz ◽  
Toshiyuki Hamaoka ◽  
Baruj Benacerraf
Keyword(s):  
T Cell ◽  
B Cells ◽  
Cell Function ◽  
Critical Role ◽  
Tolerance Induction ◽  
Immunological Tolerance ◽  
Antigenic Determinants ◽  
Humoral Responses

The present studies were designed to probe the role(s) of T cells in preventing or altering tolerance induction in hapten-specific B cells. This was accomplished by using hapten conjugates of normally immunogenic heterologous carriers to selectively inhibit 2,4-dinitrophenyl (DNP)-primed B cells in adoptive transfer experiments in vivo. The data provide strong indications that one critical role of T-cell participation in humoral responses to antigens is to circumvent the development of a tolerogenic signal that, in the absence of such T-cell function, might otherwise ensue after binding of the antigenic determinants by specific precursor B lymphocytes.

scholarly journals PR-domain–containing Mds1-Evi1 is critical for long-term hematopoietic stem cell function

Blood ◽  
2011 ◽  
Vol 118 (14) ◽  
pp. 3853-3861 ◽  
Author(s):  
Yi Zhang ◽  
Sandra Stehling-Sun ◽  
Kimberly Lezon-Geyda ◽  
Subhash C. Juneja ◽  
Lucie Coillard ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Function ◽  
Critical Role ◽  
Growth Control ◽  
Cell Compartment ◽  
Hematopoietic Stem ◽  
Stem Cell Compartment ◽  
Pr Domain

Abstract The Mds1 and Evi1 complex locus (Mecom) gives rise to several alternative transcripts implicated in leukemogenesis. However, the contribution that Mecom-derived gene products make to normal hematopoiesis remains largely unexplored. To investigate the role of the upstream transcription start site of Mecom in adult hematopoiesis, we created a mouse model with a lacZ knock-in at this site, termed MEm1, which eliminates Mds1-Evi1 (ME), the longer, PR-domain–containing isoform produced by the gene (also known as PRDM3). β-galactosidase–marking studies revealed that, within hematopoietic cells, ME is exclusively expressed in the stem cell compartment. ME deficiency leads to a reduction in the number of HSCs and a complete loss of long-term repopulation capacity, whereas the stem cell compartment is shifted from quiescence to active cycling. Genetic exploration of the relative roles of endogenous ME and EVI1 isoforms revealed that ME preferentially rescues long-term HSC defects. RNA-seq analysis in Lin−Sca-1+c-Kit+ cells (LSKs) of MEm1 documents near complete silencing of Cdkn1c, encoding negative cell-cycle regulator p57-Kip2. Reintroduction of ME into MEm1 LSKs leads to normalization of both p57-Kip2 expression and growth control. Our results clearly demonstrate a critical role of PR-domain–containing ME in linking p57-kip2 regulation to long-term HSC function.

The critical role of mast cell-derived hypoxia-inducible factor-1α in regulating mast cell function

2016 ◽  
Vol 68 (11) ◽  
pp. 1409-1416 ◽  
Author(s):  
Xin Liang ◽  
Guifang Yin ◽  
Yuanyuan Ma ◽  
Ke Xu ◽  
Jianwen Liu ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Function ◽  
Critical Role ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α
Sign in / Sign up

Export Citation Format

Share Document