Research output: Contribution to journal › Review article › peer-review
Th17 Cells, Glucocorticoid Resistance, and Depression. / Khantakova, Julia N; Mutovina, Anastasia; Ayriyants, Kseniya A et al.
In: Cells, Vol. 12, No. 23, 2749, 30.11.2023.Research output: Contribution to journal › Review article › peer-review
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TY - JOUR
T1 - Th17 Cells, Glucocorticoid Resistance, and Depression
AU - Khantakova, Julia N
AU - Mutovina, Anastasia
AU - Ayriyants, Kseniya A
AU - Bondar, Natalia P
N1 - This study was supported by the Russian Science Foundation (grant # 21-15-00142).
PY - 2023/11/30
Y1 - 2023/11/30
N2 - Depression is a severe mental disorder that disrupts mood and social behavior and is one of the most common neuropsychological symptoms of other somatic diseases. During the study of the disease, a number of theories were put forward (monoamine, inflammatory, vascular theories, etc.), but none of those theories fully explain the pathogenesis of the disease. Steroid resistance is a characteristic feature of depression and can affect not only brain cells but also immune cells. T-helper cells 17 type (Th17) are known for their resistance to the inhibitory effects of glucocorticoids. Unlike the inhibitory effect on other subpopulations of T-helper cells, glucocorticoids can enhance the differentiation of Th17 lymphocytes, their migration to the inflammation, and the production of IL-17A, IL-21, and IL-23 in GC-resistant disease. According to the latest data, in depression, especially the treatment-resistant type, the number of Th17 cells in the blood and the production of IL-17A is increased, which correlates with the severity of the disease. However, there is still a significant gap in knowledge regarding the exact mechanisms by which Th17 cells can influence neuroinflammation in depression. In this review, we discuss the mutual effect of glucocorticoid resistance and Th17 lymphocytes on the pathogenesis of depression.
AB - Depression is a severe mental disorder that disrupts mood and social behavior and is one of the most common neuropsychological symptoms of other somatic diseases. During the study of the disease, a number of theories were put forward (monoamine, inflammatory, vascular theories, etc.), but none of those theories fully explain the pathogenesis of the disease. Steroid resistance is a characteristic feature of depression and can affect not only brain cells but also immune cells. T-helper cells 17 type (Th17) are known for their resistance to the inhibitory effects of glucocorticoids. Unlike the inhibitory effect on other subpopulations of T-helper cells, glucocorticoids can enhance the differentiation of Th17 lymphocytes, their migration to the inflammation, and the production of IL-17A, IL-21, and IL-23 in GC-resistant disease. According to the latest data, in depression, especially the treatment-resistant type, the number of Th17 cells in the blood and the production of IL-17A is increased, which correlates with the severity of the disease. However, there is still a significant gap in knowledge regarding the exact mechanisms by which Th17 cells can influence neuroinflammation in depression. In this review, we discuss the mutual effect of glucocorticoid resistance and Th17 lymphocytes on the pathogenesis of depression.
KW - T-helper 17 lymphocites
KW - depression
KW - glucocorticoid resistance
KW - gut–brain axis
KW - interleukin-17
KW - neuroinflammation
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85179183166&origin=inward&txGid=1adf154f088d83a5a185e0fc08ee79f5
UR - https://www.mendeley.com/catalogue/2bc79459-713a-39af-b091-b9d4c0e8774a/
U2 - 10.3390/cells12232749
DO - 10.3390/cells12232749
M3 - Review article
C2 - 38067176
VL - 12
JO - Cells
JF - Cells
SN - 2073-4409
IS - 23
M1 - 2749
ER -
ID: 59330839