scholarly journals OX40L–OX40 Signaling in Atopic Dermatitis

2021 ◽  
Vol 10 (12) ◽  
pp. 2578
Author(s):  
Masutaka Furue ◽  
Mihoko Furue
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
T Helper 1 ◽  
Therapeutic Success ◽  
T Helper 2 ◽  
Promising Target ◽  
Antigen Presenting

OX40 is one of the co-stimulatory molecules expressed on T cells, and it is engaged by OX40L, primarily expressed on professional antigen-presenting cells such as dendritic cells. The OX40L–OX40 axis is involved in the sustained activation and expansion of effector T and effector memory T cells, but it is not active in naïve and resting memory T cells. Ligation of OX40 by OX40L accelerates both T helper 1 (Th1) and T helper 2 (Th2) effector cell differentiation. Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis.

scholarly journals Activation of central/effector memory T cells and T-helper 1 polarization in malignant melanoma patients treated with anti-programmed death-1 antibody

2018 ◽  
Vol 109 (10) ◽  
pp. 3032-3042 ◽  
Author(s):  
Kyoko Yamaguchi ◽  
Koji Mishima ◽  
Hirofumi Ohmura ◽  
Fumiyasu Hanamura ◽  
Mamoru Ito ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
T Helper 1 ◽  
Effector Memory T Cells ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Melanoma Patients ◽  
Central Effector

Remission of Alopecia Universalis after 1 Year of Treatment with Dupilumab in a Patient with Severe Atopic Dermatitis

2021 ◽  
pp. 1-4
Author(s):  
Maurizio Romagnuolo ◽  
Mauro Barbareschi ◽  
Simona Tavecchio ◽  
Luisa Angileri ◽  
Silvia Mariel Ferrucci
Keyword(s):  
Atopic Dermatitis ◽  
Skin Disorder ◽  
Human Monoclonal Antibody ◽  
Severe Atopic Dermatitis ◽  
T Helper ◽  
T Helper 1 ◽  
Th2 Response ◽  
Alopecia Universalis ◽  
T Helper 2 ◽  
Relapsing Remitting

Alopecia areata (AA), an autoimmune disease with a relapsing-remitting course, represents the second cause of non­scarring alopecia worldwide and is associated with several comorbidities, notably atopic dermatitis (AD). In particular, AD is related to its more severe forms alopecia totalis (AT) and alopecia universalis (AU) [Nat Rev Dis Primers. 2017;3:17011]. Considering that AA has been classified as T helper 1-driven disease, whereas AD is the prototypical T helper 2 (Th2)-driven skin disorder, recent studies suggest that these forms may underlie a different chemokine expression resulting in a Th2 skewing as a key pathomechanism that could explain this association [JAMA Dermatol. 2015 May;151(5):522–8]. Several reports showed that dupilumab, a fully human monoclonal antibody targeting the interleukin 4α receptor and thus downregulating Th2 response, led to an improvement of AA associated with AD; most of these patients were females with AT or AU, early-onset AD, and atopic comorbidities [Exp Dermatol. 2020 Aug;29(8):726–32]. We report here a case to further support this hypothesis.

scholarly journals FOXP3+ Regulatory T Cells and T Helper 1, T Helper 2, and T Helper 17 Cells in Human Early Pregnancy Decidua1

2010 ◽  
Vol 82 (4) ◽  
pp. 698-705 ◽  
Author(s):  
Jenny Mjösberg ◽  
Göran Berg ◽  
Maria C. Jenmalm ◽  
Jan Ernerudh
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Early Pregnancy ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 17 ◽  
T Helper 17 Cells ◽  
T Helper 2

scholarly journals OX40 (CD134) Controls Memory T Helper 2 Cells that Drive Lung Inflammation

2003 ◽  
Vol 198 (2) ◽  
pp. 315-324 ◽  
Author(s):  
Shahram Salek-Ardakani ◽  
Jianxun Song ◽  
Beth S. Halteman ◽  
Amha Gebre-Hiwot Jember ◽  
Hisaya Akiba ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Costimulatory Molecule ◽  
Airway Hyperreactivity ◽  
Th2 Cells ◽  
T Helper ◽  
Cd4 Cells ◽  
T Helper 2 ◽  
Large Numbers ◽  
Draining Lymph Nodes

Asthma is caused by memory Th2 cells that often arise early in life and persist after repeated encounters with allergen. Although much is known regarding how Th2 cells develop, there is little information about the molecules that regulate memory Th2 cells after they have formed. Here we show that the costimulatory molecule OX40 is expressed on memory CD4 cells. In already sensitized animals, blocking OX40–OX40L interactions at the time of inhalation of aerosolized antigen suppressed memory effector accumulation in lung draining lymph nodes and lung, and prevented eosinophilia, airway hyperreactivity, mucus secretion, and Th2 cyto-kine production. Demonstrating that OX40 signals directly regulate memory T cells, antigen-experienced OX40-deficient T cells were found to divide initially but could not survive and accumulate in large numbers after antigen rechallenge. Thus, OX40–OX40L interactions are pivotal to the efficiency of recall responses regulated by memory Th2 cells.

Unique gene expression program of human germinal center T helper cells

Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 1952-1960 ◽  
Author(s):  
Chang H. Kim ◽  
Hyung W. Lim ◽  
Jong R. Kim ◽  
Lusijah Rott ◽  
Peter Hillsamer ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
T Cell ◽  
Germinal Center ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
Th Cells ◽  
Effector Memory T Cells ◽  
Expression Program

Abstract Gene expression profiling was used to compare the gene expression patterns of human germinal center (GC) T helper (Th) cells with other CD4+ T-cell subsets (naive, central, and effector memory T cells). GC-Th cells, specifically localized in germinal centers to help B cells, are distantly related to central and effector memory T cells in global gene expression profiles. GC-Th cells displayed substantial differences in mRNA for adhesion molecules, chemoattractant receptors, and cytokines compared with other populations. Distinct expression of transcriptional factors by GC-Th cells is consistent with the hypothesis that they may be different from other T cells in cell lineage. Interestingly, CXCL13, a critical chemokine for B-cell entry to lymphoid follicles, is one of the most highly up-regulated genes in GC-Th cells. GC-Th cells (but not other T cells) produce and secrete large amounts of functional CXCL13 upon T-cell receptor activation, a process that is dependent on costimulation, requires translation and transcription, and is dramatically enhanced by activation in the presence of GC-B cells. This study revealed for the first time the unique gene expression program of GC-Th cells.

scholarly journals Fermented fish oil suppresses T helper 1/2 cell response in a mouse model of atopic dermatitis via generation of CD4+CD25+Foxp3+ T cells

2012 ◽  
Vol 13 (1) ◽  
pp. 44 ◽  
Author(s):  
Sang-Chul Han ◽  
Gyeoung-Jin Kang ◽  
Yeong-Jong Ko ◽  
Hee-Kyoung Kang ◽  
Sang-Wook Moon ◽  
...  
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
Mouse Model ◽  
Fish Oil ◽  
Cell Response ◽  
T Helper ◽  
T Helper 1 ◽  
Fermented Fish

scholarly journals T-cell response to bacterial agents

2011 ◽  
Vol 5 (09) ◽  
pp. 640-645 ◽  
Author(s):  
Mario Milco D'Elios ◽  
Marisa Benagiano ◽  
Chiara Della Bella ◽  
Amedeo Amedei
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Response ◽  
Th2 Cells ◽  
T Helper ◽  
T Helper 1 ◽  
Cell Responses ◽  
Genetic And Environmental Factors ◽  
Bacteria And Fungi ◽  
Antigen Presenting

T-cell responses are crucial for the outcome of any infection. The type of effector T-cell reaction is determined by a complex interaction of antigen-presenting cells with naive T cells and involves genetic and environmental factors, including the type of antigen, cytokines, chemokines, co-stimulatory molecules, and signalling cascades. The decision for the immune response to go in a certain direction is based not on one signal alone, but rather on many different elements acting both synergistically and antagonistically, and through feedback loops leading to activation or inhibition of T cells. In the course of evolution different types of T cells have developed, such as T helper 1 (Th1) cells, which protect against intracellular bacteria; Th2 cells, which play a role against parasites; and Th17 cells, which face extracellular bacteria and fungi

Abstract 561: GITR Activation Promotes Regulatory CD4+ T-cell Responses and Stimulates Leukocyte Recruitment in Atherosclerotic Plaques

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Annelie Shami ◽  
Svenja Meiler ◽  
Holger Winkels ◽  
Norbert Gerdes ◽  
Esther Lutgens
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Regulatory T Cells ◽  
B Cell ◽  
Memory T Cells ◽  
Effector Memory ◽  
Wild Type ◽  
Atherosclerotic Lesions ◽  
Effector Memory T Cells ◽  
Antigen Presenting

Glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) - a costimulatory molecule - is expressed on CD4(+) effector memory T cells and regulatory T cells as well as antigen-presenting cells and mast cells; while its ligand (GITRL) is mainly found on antigen-presenting cells and endothelial cells. However, the definitive role of GITR in atherosclerosis is not fully understood. Our hypothesis is that signaling through GITR plays a vital role in atherosclerosis progression. Low-density lipoprotein receptor-deficient mice (Ldlr -/- ) with B-cell-restricted overexpression of GITRL ( Gitrl tg ) fed a high-cholesterol diet showed a profound increase in both CD4(+) effector memory T cells and regulatory T cells in secondary lymphoid organs in comparison to wild-type controls. Additionally, the number of regulatory T cells was significantly enhanced in the thymus and aorta of these mice along with increased GITRL and interleukin-2 transcript levels. Atherosclerotic lesions of Ldlr -/- Gitrl tg mice contained more total CD3 + T cells as well as Foxp3 + regulatory T cells overall, leading to significantly less severe atherosclerosis. Conversely, atherosclerosis was found to be less severe in mice deficient in apolipoprotein E and GITR (ApoE -/- GITR -/- ). Atherosclerotic lesions in these mice were found to contain less macrophages and CD3-positive T-cells. Perfusion assays using two-photon excitation microscopy revealed less wild type leukocyte adhesion on GITR-deficient endothelium, with a further reduction in adhesion by GITR-deficient leukocytes to both wild type and GITR-deficient endothelia. Finally, expression of GITR expression in human plaque tissue was significantly increased in ruptured plaques. In conclusion, these data indicate that continuous GITR stimulation through B cell GITRL acts protective in a mouse model of atherosclerosis by regulating the balance between regulatory and effector memory CD4(+) T cells, while GITR activation on endothelial cells promotes atherogenesis by stimulating leukocyte recruitment into the plaque.

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