Th1, Th17, and Th1Th17 Lymphocytes during Tuberculosis: Th1 Lymphocytes Predominate and Appear as Low-Differentiated CXCR3+CCR6+ Cells in the Blood and Highly Differentiated CXCR3+/−CCR6− Cells in the Lungs

Nikitina, I. Yu.; Panteleev, Alexander V.; Kosmiadi, George A.; Serdyuk, Yana; Nenasheva, Tatiana A.; Николаев, А. А.; Gorelova, L.A.; Radaeva, Tatiana V.; Kiseleva, Y. Y.; Bozhenko, K. V.; Lyadova, Irina V.

doi:10.4049/jimmunol.1701424

Cited by 50 publications

(50 citation statements)

References 55 publications

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“…Excessive stimulation of Th1 immunity in TB can result in pathologic inflammation 47 . In addition, type I interferons (T1-IFNs) and Th17 immunity have been recognized to be involved in TB pathogenesis 48 , 49 . Combined with the current data, GABAergic activation may contribute to host defenses and simultaneously control excessive inflammation associated with pathologic responses during bacterial infection.…”

Section: Discussionmentioning

confidence: 99%

GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections

et al. 2018

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Gamma-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the brain; however, the roles of GABA in antimicrobial host defenses are largely unknown. Here we demonstrate that GABAergic activation enhances antimicrobial responses against intracellular bacterial infection. Intracellular bacterial infection decreases GABA levels in vitro in macrophages and in vivo in sera. Treatment of macrophages with GABA or GABAergic drugs promotes autophagy activation, enhances phagosomal maturation and antimicrobial responses against mycobacterial infection. In macrophages, the GABAergic defense is mediated via macrophage type A GABA receptor (GABAAR), intracellular calcium release, and the GABA type A receptor-associated protein-like 1 (GABARAPL1; an Atg8 homolog). Finally, GABAergic inhibition increases bacterial loads in mice and zebrafish in vivo, suggesting that the GABAergic defense plays an essential function in metazoan host defenses. Our study identified a previously unappreciated role for GABAergic signaling in linking antibacterial autophagy to enhance host innate defense against intracellular bacterial infection.

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Section: Discussionmentioning

confidence: 99%

GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections

et al. 2018

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“…Более того, снижение уровня IL-17 в периферической крови больных ТБ было тесно связано с низкой эффективностью применяемой терапии и неблагоприятным исходом данного заболевания [9]. Особый интерес также представляют литературные данные о том, что более половины IFNγсекретирующих M. tuberculosis-специфических Th клеток обладают фенотипом CXCR3 + CCR6 + [20], что еще раз указывает на важную роль Th17.1 клеток в развитии иммунного ответа при туберкулезе.…”

Section: Discussionunclassified

Altered peripheral blood Th17 and follicular T-helper subsets in patients with pulmonary tuberculosis

Кудрявцев

Серебрякова

Старшинова

et al. 2019

Russian Journal of Infection and Immunity

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Tuberculosis (TB) is one of the most common infections worldwide. Eradication of an intracellular pathogen M. tuberculosis requires to induce a Th1 response by activating IFNγ-producing tissue macrophages. Along with Th1 cells, various subsets of Th17 and follicular T-helper cells (Tfh) able to secrete a broad range of cytokines, including IFNγ, can also be involved in eliminating bacterial pathogens. It justified analyzing in this study changes in percentage of various peripheral blood Th subsets, including Th1, Th2, Th17 and Tfh cells, in TB patients. For this, major CD3+CD4+T cell subsets were assessed by using multicolor flow cytometry in TB patients (n = 40) and healthy volunteers (n = 30). It was found that in TB patients vs. control group percentage of peripheral blood CD45RA–CCR7+ central memory (CM) Th was decreased also affecting frequency of some functional T cell subsets, e.g. either lowering Th2 cells (9.11% (6.95; 13.77) vs. 7.21% (5.64; 9.84), p = 0.012) or elevating CCR6+ Th17 subsets (35.92% (27.72; 41.06) vs. 40.39% (35.41; 47.79; p = 0.016), respectively, but not influencing Th1 and Tfh subsets frequencies. Moreover, percentage of total CCR6+CM Th cells in TB patients vs. control was decreased in CCR4–CXCR3+Th17.1 cell subset (42.87% (33.64; 49.45) vs. 52.26% (46.45; 56.95), p < 0.001), whereas standard CCR4+CXCR3–Th17 and CCR6+ DP Th17 subsets were elevated (p = 0.005 and p = 0.002, respectively). In addition, altered Tfh subset composition associated with the increased (p = 0.021) percentage of CXCR3–CCR6–Tfh2 cells, but decreased CXCR3+CCR6–Tfh1 cells (p = 0.036) was observed. Finally, frequency of peripheral blood Th subsets noted above was also analyzed within effector memory (CD45RA–CCR7–) cells. It was found that in TB patients vs. volunteers frequency of Th17.1 cells was also significantly lower (p = 0.006) in CCR6+EM Th (54.43% (41.19; 91.92) vs. 61.76% (54.01; 65.63), whereas percentage of double-positive Th17 was significantly increased (20.83% (15.12; 30.87) and 12.93 % (9.80; 19.01), respectively, p < 0.001). Thus, it suggests that during M. tuberculosis infection percentage of IFNγ-producing Th17 and Tfh cells was reduced compared to control group also affecting both central memory Th cells patrolling peripheral lymphoid organs as well as effector memory Th cells able to exit to site of infection.

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“…In addition, a special group of CD3 + CD4 + CD183 + CD196 + substyle is named Th1Th17. Th1Th17 is an interesting Th subset, which can produce both Th1 and Th17 cytokines, such as IFN-g and IL-17 [39,66]. Based on its cytokines, we speculate that it is a group of Th cells with stronger inflammation.…”

Section: Discussionmentioning

confidence: 99%

CRID3, a Blocker of Apoptosis Associated Speck Like Protein Containing a Card, Ameliorates Murine Spinal Cord Injury by Improving Local Immune Microenvironment

et al. 2020

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demonstrated that inflammasomes may play an important role in the inflammation of SCI. Because ASC is the adaptor protein shared by inflammasomes, we speculated that ASC can be used as a target to inhibit the activation of inflammasomes, so as to improve the local immune microenvironment of SCI and reduce nerve damage. In this study, CRID3, a blocker of ASC oligomerization [18], was used to study its effect on the local microenvironment and the possible role in neuroprotection following SCI. Methods Animals A total of 120 female C57BL/6 mice (weight, 18-20 g; age, 8 weeks old) obtained from Chang Zhou Cavens Laboratory Animal Ltd. Animals were housed in ventilated cages and maintained on a 12-hour light/dark cycle with ad libitum access to food and water. Ambient room temperature was maintained at 20 ~ 22 °C with 30 ~ 70% humidity. Animal care following surgery complied with the regulations for the management of experimental animals (revised by the Ministry of Science and Technology of China in June 2004). The study was approved by the Institutional Committee on Animal Care, Use and Research of the Bengbu Medical College. Contusive SCI and drug injection. An Infinite Horizon impactor (Precision Systems & Instrumentation) was used to perform contusive SCI, as previously described [19, 20]. The mice were first anesthetized with a cocktail of ketamine (80 mg/kg)/xylazine (10 mg/kg) intraperitoneally injection and then the T9 lamina was excised. The spine was stabilized by clamping the T7 and T11 spinous processes, and then a moderate SCI model was created using a rod (1.3 mm in diameter) with a force of 50 Kdynes. Sham-operated (sham) mice only received a laminectomy without contusive injury. Post-surgically, mice were placed in a temperature-and humidity-controlled chamber. Manual bladder emptying was performed three times daily until reflex bladder emptying was established. To prevent infections, animals were daily provided with chloramphenicol (50 mg/kg) via drinking water. The spinal cord-injured mice were randomly assigned to the vehicle control or CRID3 injection groups. Mice were intraperitoneally injected with 0.01 M PBS (pH 7.4) or CRID3 (Target Molecule Corp., 50 mg/kg prepared in PBS)

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Th1, Th17, and Th1Th17 Lymphocytes during Tuberculosis: Th1 Lymphocytes Predominate and Appear as Low-Differentiated CXCR3+CCR6+ Cells in the Blood and Highly Differentiated CXCR3+/−CCR6− Cells in the Lungs

Cited by 50 publications

References 55 publications

GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections

GABAergic signaling linked to autophagy enhances host protection against intracellular bacterial infections

Altered peripheral blood Th17 and follicular T-helper subsets in patients with pulmonary tuberculosis

CRID3, a Blocker of Apoptosis Associated Speck Like Protein Containing a Card, Ameliorates Murine Spinal Cord Injury by Improving Local Immune Microenvironment

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