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Telbivudine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Several predictors for efficacy of telbivudine treatment had been identified based on these clinical trials. Baseline HBV DNA, at levels < 9 log10 copies/ml, or ALT levels ≥ 2 above normal were strong pretreatment outcome predictors for HBeAg-positive subjects, but not for HBeAg-negative patients. However, nondetectable serum HBV DNA at treatment week 24 was the strongest predictor for better outcomes for both HBeAg-positive and -negative groups. A combination of pretreatment characteristics plus week-24 response could identify subgroups with the best outcomes (Zeuzem et al., 2009). Recently, quantitative hepatitis B core antibody (anti-HBc) as an immunological biomarker that may reflect host-adaptive anti-HBV immune activity has been shown to be a strong predictor for HBeAg seroconversion during telbivudine treatment. Higher pretreatment anti-HBc level was associated with higher rate of HBeAg seroconversion (Fan et al., 2016). Besides, level of interleukin 21 (IL-21) and frequency of circulating chemokine (C-XC motif) receptor 5 (CXCR5)+ CD4+ T-cells were also demonstrated to be related to the HBeAg seroconversion during telbivudine treatment (Ma et al., 2012; Li et al., 2013). These predictors may be used for pretreatment stratification aimed at optimizing the treatment of CHB.
Autophagy-deficiency in bone marrow mononuclear cells from patients with myasthenia gravis: a possible mechanism of pathogenesis
Published in International Journal of Neuroscience, 2021
Jingqun Tang, Ziming Ye, Yi Liu, Mengxiao Zhou, Liqiang Huang, Qin Mo, Xiaotao Su, Chao Qin
Over the last few years, there has been increasing evidence that autophagy plays an indispensable role in both the innate and adaptive immunology processes, involving intracellular pathogen recognition and removal, major histocompatibility complex (MHC) presentation, lymphocyte function and development, pro-inflammatory signalling, apoptotic cell clearance, cytokine secretory pathways, and humoural immunity processes [7–13]. Due to its functions in the immune system, autophagy might exert a pathogenic and/or therapeutic role in autoimmune diseases (AIDs) [14]. Balanced and stable autophagy is recommended for ex vivo use to ameliorate the disease activity and to improve immune dysfunction in systemic lupus erythaematosus (SLE) patients [15]. The interleukin-21 (IL-21) -induced activation of mechanistic target of rapamycin (mTOR) can further improve deficient autophagy and the differentiation of regulatory T cells (Tregs) in SLE patients [16]. Furthermore, a protective role of autophagy in inhibiting programmed cell death has been shown by the conditional knockout of beclin-1 in activated T cells in an experimental autoimmune encephalomyelitis (EAE) model [17]. Additionally, the autophagy inhibitor chloroquine (CHQ) may deteriorate psoriasis by modulating interleukin-23 (IL-23) release in a p38-dependent manner [18]. In summary, autophagy is inseparable from the development of AIDs.
ER-stressed MSC displayed more effective immunomodulation in RA CD4+CXCR5+ICOS+ follicular helper-like T cells through higher PGE2 binding with EP2/EP4
Published in Modern Rheumatology, 2020
Jing Wei, Xunli Ouyang, Yawei Tang, Han Li, Bing Wang, Yunshan Ye, Minli Jin, Mahmoud Al Azab, Weiping Li, Xia Li
Rheumatoid arthritis (RA) is characterized by persistent articular inflammation and synovitis, leading to progressive cartilage and joint destruction. Tfh cells, specialized in assisting B cells with antibody production [1], are considered to be a novel subtype of CD4+ T cells, which mainly localize to B-cell follicles in secondary lymphoid tissues and express phenotypic molecules, such as C-X-C chemokine receptor 5 (CXCR5), inducible costimulatory molecule (ICOS), CD40 ligand and interleukin-21 (IL-21). Excessive Tfh cells response is likely to result in many autoimmune diseases including systemic lupus erythematosus (SLE) and RA [2,3]. Blocking Tfh cells function was regarded as an effective strategy in the treatment of some autoimmune diseases [4]. As suggested by our study and others, circulating Tfh cell proportions were elevated in RA patients and were positively correlated with disease activity [5,6]. Interestingly, therapies targeting Tfh cells have been shown to dramatically ameliorate RA syndrome [7]. So inhibition of Tfh cells is a promising treatment target for RA treatment.
Effect of IL-21 on the Balance of Th17 Cells/Treg Cells in the Pathogenesis of Graves’ Disease
Published in Endocrine Research, 2019
Yan Tan, Wei Chen, Chun Liu, Xiaoya Zheng, Ai Guo, Jian Long
The immune balance of Th17/Treg cells has been implicated in autoimmune diseases.14–17 However, the studies of GD pathogenesis have emphasized the influence of Th17 cells or Treg cells, rather than the balance of Th17/Treg cells. Therefore, the role of the Th17/Treg cell balance in the pathogenesis of GD and the regulatory mechanism of IL-21 in the Th17/Treg balance in GD are of great importance. In this study, the role of IL-21 in regulating the immune balance of Th17/Treg cells in the pathogenesis of GD was preliminarily explored by detecting the levels of the transcription factor RORγt, the cytokines IL-17 and IL-22, the Treg cell-specific transcription factor Foxp3, and the cytokine IL-10 in peripheral blood mononuclear cells (PBMCs) with and without recombinant human interleukin-21 (rhIL-21) stimulation.