scholarly journals The role of EMMPRIN in T cell biology and immunological diseases

2015 ◽  
Vol 98 (1) ◽  
pp. 33-48 ◽  
Author(s):  
Jennifer Nancy Hahn ◽  
Deepak Kumar Kaushik ◽  
V. Wee Yong
Keyword(s):  
T Cell ◽  
Cell Biology ◽  
T Cell Biology ◽  
Immunological Diseases

scholarly journals T Cell Receptor Specificity Is Critical for the Development of Epidermal γδ T Cells

2001 ◽  
Vol 194 (10) ◽  
pp. 1473-1483 ◽  
Author(s):  
Isabel Ferrero ◽  
Anne Wilson ◽  
Friedrich Beermann ◽  
Werner Held ◽  
H. Robson MacDonald
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Biology ◽  
Γδ T Cells ◽  
Cell Receptor ◽  
Wild Type ◽  
Normal Numbers ◽  
T Cell Biology

A particular feature of γδ T cell biology is that cells expressing T cell receptor (TCR) using specific Vγ/Vδ segments are localized in distinct epithelial sites, e.g., in mouse epidermis nearly all γδ T cells express Vγ3/Vδ1. These cells, referred to as dendritic epidermal T cells (DETC) originate from fetal Vγ3+ thymocytes. The role of γδ TCR specificity in DETC's migration/localization to the skin has remained controversial. To address this issue we have generated transgenic (Tg) mice expressing a TCR δ chain (Vδ6.3-Dδ1-Dδ2-Jδ1-Cδ), which can pair with Vγ3 in fetal thymocytes but is not normally expressed by DETC. In wild-type (wt) Vδ6.3Tg mice DETC were present and virtually all of them express Vδ6.3. However, DETC were absent in TCR-δ−/− Vδ6.3Tg mice, despite the fact that Vδ6.3Tg γδ T cells were present in normal numbers in other lymphoid and nonlymphoid tissues. In wt Vδ6.3Tg mice, a high proportion of in-frame Vδ1 transcripts were found in DETC, suggesting that the expression of an endogenous TCR-δ (most probably Vδ1) was required for the development of Vδ6.3+ epidermal γδ T cells. Collectively our data demonstrate that TCR specificity is essential for the development of γδ T cells in the epidermis. Moreover, they show that the TCR-δ locus is not allelically excluded.

scholarly journals Role of Inositol Poly-Phosphatases and Their Targets in T Cell Biology

2013 ◽  
Vol 4 ◽  
Author(s):  
Neetu Srivastava ◽  
Raki Sudan ◽  
William Garrow Kerr
Keyword(s):  
T Cell ◽  
Cell Biology ◽  
T Cell Biology

scholarly journals T cell factor 1: A master regulator of the T cell response in disease

2020 ◽  
Vol 5 (53) ◽  
pp. eabb9726
Author(s):  
Giulia Escobar ◽  
Davide Mangani ◽  
Ana C. Anderson
Keyword(s):  
T Cell ◽  
Cell Biology ◽  
T Cell Development ◽  
Memory Formation ◽  
T Cell Response ◽  
Chronic Infections ◽  
T Cell Factor ◽  
T Cell Biology ◽  
Peripheral T Cells

Recent advances have redefined a role for T cell factor 1 (TCF1) that goes beyond T cell development and T memory formation and encompasses new functions in the regulation of T cell biology. Here, we discuss the multifaceted and context-dependent role of TCF1 in peripheral T cells, particularly during disease-induced inflammatory states such as autoimmunity, cancer, and chronic infections. Understanding how TCF1 fine-tunes peripheral T cell biology holds the potential to tailor improved immune-targeted therapies.

scholarly journals Role of the Orphan Nuclear Receptor NR4A Family in T-Cell Biology

2021 ◽  
Vol 11 ◽  
Author(s):  
Livia Odagiu ◽  
Julia May ◽  
Salix Boulet ◽  
Troy A. Baldwin ◽  
Nathalie Labrecque
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Biology ◽  
Cell Receptor ◽  
Antigen Recognition ◽  
Orphan Nuclear Receptor ◽  
Orphan Receptors ◽  
Cell Responses ◽  
T Cell Biology

The nuclear orphan receptors NR4A1, NR4A2, and NR4A3 are immediate early genes that are induced by various signals. They act as transcription factors and their activity is not regulated by ligand binding and are thus regulated via their expression levels. Their expression is transiently induced in T cells by triggering of the T cell receptor following antigen recognition during both thymic differentiation and peripheral T cell responses. In this review, we will discuss how NR4A family members impact different aspects of the life of a T cell from thymic differentiation to peripheral response against infections and cancer.

scholarly journals The Role of Protein Kinase Cη in T Cell Biology

2012 ◽  
Vol 3 ◽  
Author(s):  
Guo Fu ◽  
Nicholas R. J. Gascoigne
Keyword(s):  
T Cell ◽  
Protein Kinase ◽  
Cell Biology ◽  
T Cell Biology

scholarly journals Beyond T-Cells: Functional Characterization of CTLA-4 Expression in Immune and Non-Immune Cell Types

2020 ◽  
Vol 11 ◽  
Author(s):  
Damilola Oyewole-Said ◽  
Vanaja Konduri ◽  
Jonathan Vazquez-Perez ◽  
Scott A. Weldon ◽  
Jonathan M. Levitt ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Cell Biology ◽  
Functional Characterization ◽  
Costimulatory Molecule ◽  
T Cell Response ◽  
Direct Result ◽  
T Cell Biology

The immune response consists of a finely-tuned program, the activation of which must be coupled with inhibitory mechanisms whenever initiated. This ensures tight control of beneficial anti-pathogen and anti-tumor responses while preserving tissue integrity, promoting tissue repair, and safeguarding against autoimmunity. A cogent example of this binary response is in the mobilization of co-stimulatory and co-inhibitory signaling in regulating the strength and type of a T-cell response. Of particular importance is the costimulatory molecule CD28 which is countered by CTLA-4. While the role of CD28 in the immune response has been thoroughly elucidated, many aspects of CTLA-4 biology remain controversial. The expression of CD28 is largely constrained to constitutive expression in T-cells and as such, teasing out its function has been somewhat simplified by a limited and specific expression profile. The expression of CTLA-4, on the other hand, while reported predominantly in T-cells, has also been described on a diverse repertoire of cells within both lymphoid and myeloid lineages as well as on the surface of tumors. Nonetheless, the function of CTLA-4 has been mostly described within the context of T-cell biology. The focus on T-cell biology may be a direct result of the high degree of amino acid sequence homology and the co-expression pattern of CD28 and CTLA-4, which initially led to the discovery of CTLA-4 as a counter receptor to CD28 (for which a T-cell-activating role had already been described). Furthermore, observations of the outsized role of CTLA-4 in Treg-mediated immune suppression and the striking phenotype of T-cell hyperproliferation and resultant disease in CTLA-4−/− mice contribute to an appropriate T-cell-centric focus in the study of CTLA-4. Complete elucidation of CTLA-4 biology, however, may require a more nuanced understanding of its role in a context other than that of T-cells. This makes particular sense in light of the remarkable, yet limited utility of anti-CTLA-4 antibodies in the treatment of cancers and of CTLA-4-Ig in autoimmune disorders like rheumatoid arthritis. By fully deducing the biology of CTLA-4-regulated immune homeostasis, bottlenecks that hinder the widespread applicability of CTLA-4-based immunotherapies can be resolved.

scholarly journals Human Wnt/β-Catenin Regulates Alloimmune Signaling during Allogeneic Transplantation

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3798
Author(s):  
Mahinbanu Mammadli ◽  
Rebecca Harris ◽  
Sara Mahmudlu ◽  
Anjali Verma ◽  
Adriana May ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Biology ◽  
Allogeneic Transplantation ◽  
Hematopoietic Stem ◽  
Inflammatory Cytokine Production ◽  
Formidable Challenge ◽  
T Cell Biology ◽  
Donor T Cells

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is one of the most widely applied forms of adoptive immunotherapy for the treatment of hematological malignancies. Detrimental graft-versus-host disease (GVHD), but also beneficial graft-versus-leukemia (GVL) effects occurring after allo-HSCT are largely mediated by alloantigen-reactive donor T cells in the graft. Separating GVHD from GVL effects is a formidable challenge, and a greater understanding of donor T cell biology is required to accomplish the uncoupling of GVHD from GVL. Here, we evaluated the role of β-catenin in this process. Using a unique mouse model of transgenic overexpression of human β-catenin (Cat-Tg) in an allo-HSCT model, we show here that T cells from Cat-Tg mice did not cause GVHD, and surprisingly, Cat-Tg T cells maintained the GVL effect. Donor T cells from Cat-Tg mice exhibited significantly lower inflammatory cytokine production and reduced donor T cell proliferation, while upregulating cytotoxic mediators that resulted in enhanced cytotoxicity. RNA sequencing revealed changes in the expression of 1169 genes for CD4, and 1006 genes for CD8+ T cells involved in essential aspects of immune response and GVHD pathophysiology. Altogether, our data suggest that β-catenin is a druggable target for developing therapeutic strategies to reduce GVHD while preserving the beneficial GVL effects following allo-HSCT treatment.

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