Abstract：
BACKGROUND: Major depressive disorder (MDD) is characterized by increased T helper (Th)1 polarization, T cell activation (e.g., CD71+ and CD40L+), and cannabinoid receptor type 2 bearing CD20+ B cells; and lower T regulatory (Treg) numbers.
OBJECTIVE: To delineate the effects of adverse childhood experiences (ACEs) and recurrence of illness (ROI) on activated T and CB2-bearing B populations, and Tregs, including FoxP3 + CD152+, FoxP3 + GARP+, and FoxP3 + CB1+ cells.
METHODS: We measured ROI, ACEs, the number of activated T cells, Tregs, and CD20 + CB2+ B cells, in 30 MDD patients and 20 healthy controls.
RESULTS: A larger part of the variance in the depression phenome (40.8 %) was explained by increased CD20 + CB2+ and activated T cells, and lowered Tregs. ROI and lifetime suicidal behaviors were significantly and positively associated with CD20 + CB2+, CD3 + CD71+, CD3 + CD40L+, CD4 + CD71+, CD4 + CD40L+, and CD4HLADR+ numbers. ROI was significantly correlated with CD8 + CD40L+ numbers. The sum of ACEs was significantly associated with CD20 + CB2+, CD3 + CD40L+, CD4 + 40 L+ numbers, T cell activation (positively) and Treg (inversely) indices. One replicable latent vector could be extracted from activated T cells, lifetime and current suicidal behaviors, number of depressive episodes, and severity of depression, and 48.8 % of its variance was explained by ACEs.
CONCLUSIONS: ACE-induced activation of T effector and cytotoxic cells and B cells with autoimmune potential, coupled with lowered Treg numbers are a key component of depression. The findings indicate that increasing ROI, the phenome of depression and suicidal behaviors, are caused by autoimmune processes, which are the consequence of ACEs and increasing sensitization of immune responses.
OBJECTIVE: To delineate the effects of adverse childhood experiences (ACEs) and recurrence of illness (ROI) on activated T and CB2-bearing B populations, and Tregs, including FoxP3 + CD152+, FoxP3 + GARP+, and FoxP3 + CB1+ cells.
METHODS: We measured ROI, ACEs, the number of activated T cells, Tregs, and CD20 + CB2+ B cells, in 30 MDD patients and 20 healthy controls.
RESULTS: A larger part of the variance in the depression phenome (40.8 %) was explained by increased CD20 + CB2+ and activated T cells, and lowered Tregs. ROI and lifetime suicidal behaviors were significantly and positively associated with CD20 + CB2+, CD3 + CD71+, CD3 + CD40L+, CD4 + CD71+, CD4 + CD40L+, and CD4HLADR+ numbers. ROI was significantly correlated with CD8 + CD40L+ numbers. The sum of ACEs was significantly associated with CD20 + CB2+, CD3 + CD40L+, CD4 + 40 L+ numbers, T cell activation (positively) and Treg (inversely) indices. One replicable latent vector could be extracted from activated T cells, lifetime and current suicidal behaviors, number of depressive episodes, and severity of depression, and 48.8 % of its variance was explained by ACEs.
CONCLUSIONS: ACE-induced activation of T effector and cytotoxic cells and B cells with autoimmune potential, coupled with lowered Treg numbers are a key component of depression. The findings indicate that increasing ROI, the phenome of depression and suicidal behaviors, are caused by autoimmune processes, which are the consequence of ACEs and increasing sensitization of immune responses.
摘要：
背景：重度抑郁症（MDD）的特征是T辅助（Th）1极化增加，T细胞活化(例如，CD71+和CD40L+),和携带CD20+B细胞的2型大麻素受体;和较低的T调节(Treg)数量。
目的：描述不良儿童经历（ACE）和疾病复发（ROI）对活化T和CB2携带B人群的影响，和Tregs,包括FoxP3+CD152+，FoxP3+GARP+,和FoxP3+CB1+细胞。
方法：我们测量了ROI，ACE,激活的T细胞的数量，Tregs,和CD20+CB2+B细胞，30例MDD患者和20例健康对照。
结果：抑郁症表型变异的较大部分（40.8％）是由CD20+CB2+和活化的T细胞增加解释的，降低Tregs.ROI和终生自杀行为与CD20+CB2+显著正相关，CD3+CD71+,CD3+CD40L+,CD4+CD71+,CD4+CD40L+,和CD4HLADR+数字。ROI与CD8+CD40L+数量显著相关。ACEs的总和与CD20+CB2+显著相关，CD3+CD40L+,CD4+40L+数字，T细胞活化(正)和Treg(逆)指数。可以从活化的T细胞中提取一种可复制的潜伏载体，一生和当前的自杀行为，抑郁发作的次数，和抑郁症的严重程度，其48.8%的变异由ACE解释。
结论：ACE诱导的T效应细胞和细胞毒性细胞以及具有自身免疫潜能的B细胞的活化，再加上降低的Treg数量是抑郁症的关键组成部分。研究结果表明，提高投资回报率，抑郁症和自杀行为的现象，是由自身免疫过程引起的，这是ACEs和免疫应答敏化增加的结果。
目的：描述不良儿童经历（ACE）和疾病复发（ROI）对活化T和CB2携带B人群的影响，和Tregs,包括FoxP3+CD152+，FoxP3+GARP+,和FoxP3+CB1+细胞。
方法：我们测量了ROI，ACE,激活的T细胞的数量，Tregs,和CD20+CB2+B细胞，30例MDD患者和20例健康对照。
结果：抑郁症表型变异的较大部分（40.8％）是由CD20+CB2+和活化的T细胞增加解释的，降低Tregs.ROI和终生自杀行为与CD20+CB2+显著正相关，CD3+CD71+,CD3+CD40L+,CD4+CD71+,CD4+CD40L+,和CD4HLADR+数字。ROI与CD8+CD40L+数量显著相关。ACEs的总和与CD20+CB2+显著相关，CD3+CD40L+,CD4+40L+数字，T细胞活化(正)和Treg(逆)指数。可以从活化的T细胞中提取一种可复制的潜伏载体，一生和当前的自杀行为，抑郁发作的次数，和抑郁症的严重程度，其48.8%的变异由ACE解释。
结论：ACE诱导的T效应细胞和细胞毒性细胞以及具有自身免疫潜能的B细胞的活化，再加上降低的Treg数量是抑郁症的关键组成部分。研究结果表明，提高投资回报率，抑郁症和自杀行为的现象，是由自身免疫过程引起的，这是ACEs和免疫应答敏化增加的结果。
