scholarly journals Origin, function and role in the development of skin diseases CLA+T-lymphocytes

2018 ◽  
Vol 94 (3) ◽  
pp. 20-29
Author(s):  
A. V. Patrushev ◽  
A. V. Samtsov ◽  
V. Yu. Nikitin ◽  
A. М. Ivanov ◽  
O. Р. Gumilevskaya ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Skin Diseases ◽  
Memory T Cells ◽  
Detailed Understanding ◽  
Malignant Skin Tumors ◽  
Malignant Skin ◽  
Functional Features ◽  
Origin Function

The idea of CLA+T-lymphocytes, which are a special subpopulation of cells with a tropic to the skin, is given. The issues of maturation, migration and functional features of CLA+T-cells are considered. Special attention is paid to the different phenotype of memory T-cells. Modern data concerning the role of CLA+T-cells in the pathogenesis of autoimmune and allergic dermatoses, as well as malignant skin tumors are also presented. The conclusion about the necessity of further study of CLA +T-lymphocytes for detailed understanding of pathogenesis and search of variants of targeted therapy in psoriasis, atopic dermatitis, skin lymphomas and other skin diseases is made.

scholarly journals Tissue-Resident Memory T Cells in Skin Diseases: A Systematic Review

2021 ◽  
Vol 22 (16) ◽  
pp. 9004
Author(s):  
Thomas Emmanuel ◽  
Josephine Mistegård ◽  
Anne Bregnhøj ◽  
Claus Johansen ◽  
Lars Iversen
Keyword(s):  
T Cells ◽  
Skin Diseases ◽  
Memory T Cells ◽  
Future Research ◽  
Inclusion Criteria ◽  
Local Skin ◽  
Resident Memory T Cells ◽  
Infectious Skin Diseases

In health, the non-recirculating nature and long-term persistence of tissue-resident memory T cells (TRMs) in tissues protects against invading pathogens. In disease, pathogenic TRMs contribute to the recurring traits of many skin diseases. We aimed to conduct a systematic literature review on the current understanding of the role of TRMs in skin diseases and identify gaps as well as future research paths. EMBASE, PubMed, SCOPUS, Web of Science, Clinicaltrials.gov and WHO Trials Registry were searched systematically for relevant studies from their inception to October 2020. Included studies were reviewed independently by two authors. This study was conducted in accordance with the PRISMA-S guidelines. This protocol was registered with the PROSPERO database (ref: CRD42020206416). We identified 96 studies meeting the inclusion criteria. TRMs have mostly been investigated in murine skin and in relation to infectious skin diseases. Pathogenic TRMs have been characterized in various skin diseases including psoriasis, vitiligo and cutaneous T-cell lymphoma. Studies are needed to discover biomarkers that may delineate TRMs poised for pathogenic activity in skin diseases and establish to which extent TRMs are contingent on the local skin microenvironment. Additionally, future studies may investigate the effects of current treatments on the persistence of pathogenic TRMs in human skin.

Role of Memory T Cells in Influenza Viral Infection

2008 ◽  
Vol 7 (2) ◽  
pp. 87-96
Author(s):  
Rabih Halwani ◽  
Mehrnoosh Doroudchi ◽  
Mohamed El-Far ◽  
Andre Tanel ◽  
Yu Shi ◽  
...  
Keyword(s):  
T Cells ◽  
Viral Infection ◽  
Memory T Cells ◽  
Influenza Viral Infection

Abstract P332: Role of T-Lymphocytes in the Long-Term Blood Pressure and Renal Disease Effects of Acute Renal Ischemia-Reperfusion Injury

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Bernardo Lopez ◽  
Galina Petrova ◽  
Justine M Abais-Battad ◽  
Hayley Lund ◽  
Daniel Fehrenbach ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Renal Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Immunosuppressive Agents ◽  
High Salt ◽  
Renal Ischemia ◽  
Salt Sensitive Hypertension

Epidemiological data indicates that acute kidney injury (AKI) is an independent risk factor for the development of hypertension and chronic kidney disease in patients. Previous studies demonstrated that rats develop sodium-dependent hypertension and kidney damage following experimental AKI induced by a renal ischemia-reperfusion (IR) insult; furthermore, these high salt deleterious effects could be blunted by administration of immunosuppressive agents. The present study was performed on Dahl SS (SS) rats and SS rats with a null mutation in the CD247 gene (SS-CD247) leading to depletion of T-lymphocytes in order to specifically examine the role of T cells in this response (n=5-6 rats/group). As assessed by serum creatinine (SCr) levels, no difference was observed in the initial response to IR injury between SS and SS-CD247: SCr increased from 0.44±0.03 to 2.16±0.32 mg/dl in SS rats 24 hours after an initial 30 minute period of renal ischemia and returned to control levels after 8 days of recovery. Moreover, no differences were noted in mean arterial pressure (MAP) or albumin excretion rate (UAlb) between SS and SS-CD247 after 43 days of recovery from IR injury while the rats were maintained on a low salt (0.4% NaCl) diet. When the rats were fed a 4.0% NaCl diet for two weeks, MAP and UAlb significantly increased in the sham SS to 178±9 mmHg and 189±25 mg/day, respectively; values significantly greater than observed in the sham SS-CD247 rats (148±2 mmHg and 87±17 mg/day). As expected, the SS rats recovered from IR injury demonstrated an exaggerated increase in MAP (peaking at 183±2 mmHg) and UAlb (275±54 mg/day) in response to high salt. There was no difference in the number of total CD3+ lymphocytes in the kidneys of IR and sham SS after high salt, though the ratio of CD4+/CD8+ T cells was increased in the IR group. Compared to sham CD247, an exaggerated elevation of MAP (157±9 mmHg) and UAlb (210±32 mg/day) was also observed in the SS-CD247 rats recovered from IR injury, demonstrating enhanced responsiveness following IR injury in animals lacking T cells. These data indicate that T lymphocytes amplify salt-sensitive hypertension and renal damage, but other mechanisms also mediate the salt-sensitive hypertension and renal damage that occurs in animals recovered from IR injury.

scholarly journals Memory T cells are anergic to the superantigen staphylococcal enterotoxin B.

1992 ◽  
Vol 176 (2) ◽  
pp. 575-579 ◽  
Author(s):  
W T Lee ◽  
E S Vitetta
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Staphylococcal Enterotoxin ◽  
Peripheral Tolerance ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B

We have used staphylococcal enterotoxin B (SEB) to study the role of naive and memory T cells in the induction of peripheral tolerance. After administration of SEB to mice, the numbers of naive and memory T cells increase, as does the proportion of memory T cells, which are unresponsive to further stimulation with SEB in vitro. In addition, memory T cells generated in response to conventional antigen, which proliferate and provide help to B cells in the presence of the conventional antigen, fail to respond to superantigen. Hence, memory T cells, in general, are anergized by SEB. These results suggest that SEB-induced activation and anergy reflect the combined responses of naive and memory T cells. The differential activation vs. anergy of naive and memory T cells by superantigen may be related to cytokine production and may play an important role in the etiology of autoimmune diseases or immunodeficiency diseases such as acquired immune deficiency syndrome.

scholarly journals The influence of chorionic gonadotropin on phenotype conversion and hTERT gene expression by T-lymphocytes of different degrees of differentiation

2017 ◽  
Vol 63 (6) ◽  
pp. 539-545 ◽  
Author(s):  
M.B. Rayev ◽  
S.A. Zamorina ◽  
L.S. Litvinova ◽  
K.A. Yurova ◽  
O.G. Khaziakhmatova ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Chorionic Gonadotropin ◽  
Memory T Cells ◽  
Immune Memory ◽  
Proliferation Marker ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Htert Gene

The effects of chorionic gonadotropin (hCG) on the expression of the hTERT gene in combination with the conversion of the phenotype of naive T-cells and T-cells of immune memory in vitro were studied. hCG inhibited expression of hTERT mRNA in naive T-cells (CD45RA+) and immune memory T cells (CD45RO+), causing a decrease in the replicative potential of the cells. The presence of hCG in the culture led to the conversion of the phenotype of T-lymphocytes. hCG reduced the number of proliferating T-cells of immune memory, estimated by phenotypic signs by differential gating. hCG (10 IU/ml and 100 IU/ml) inhibited expression of CD25 by the studied populations, but did not modulate expression of the CD71 proliferation marker. Thus, hCG inhibited the functional activity of naive T-cells and T-cells of immune memory, which, in the context of pregnancy, can contribute to the formation of immune tolerance to the semi-allogenic fetus.

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