Kidd Parris
Altern Med Rev. 2003 Aug;8(3):223-46.
One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and T-helper 2 (Th2) activity. The Th1/Th2 hypothesis arose from 1986 research suggesting mouse T-helper cells expressed differing cytokine patterns. This hypothesis was adapted to human immunity, with Th1- and Th2-helper cells directing different immune response pathways. Th1 cells drive the type-1 pathway ("cellular immunity") to fight viruses and other intracellular pathogens, eliminate cancerous cells, and stimulate delayed-type hypersensitivity (DTH) skin reactions. Th2 cells drive the type-2 pathway ("humoral immunity") and up-regulate antibody production to fight extracellular organisms; type 2 dominance is credited with tolerance of xenografts and of the fetus during pregnancy. Overactivation of either pattern can cause disease, and either pathway can down-regulate the other. But the hypothesis has major inconsistencies; human cytokine activities rarely fall into exclusive pro-Th1 or -Th2 patterns. The non-helper regulatory T cells, or the antigen-presenting cells (APC), likely influence immunity in a manner comparable to Th1 and Th2 cells. Many diseases previously classified as Th1 or Th2 dominant fail to meet the set criteria. Experimentally, Th1 polarization is readily transformed to Th2 dominance through depletion of intracellular glutathione, and vice versa. Mercury depletes glutathione and polarizes toward Th2 dominance. Several nutrients and hormones measurably influence Th1/Th2 balance, including plant sterols/sterolins, melatonin, probiotics, progesterone, and the minerals selenium and zinc. The long-chain omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) significantly benefit diverse inflammatory and autoimmune conditions without any specific Th1/Th2 effect. Th1/Th2-based immunotherapies, e.g., T-cell receptor (TCR) peptides and interleukin-4 (IL-4) injections, have produced mixed results to date.
一种免疫调节理论涉及辅助性T细胞1（Th1）和辅助性T细胞2（Th2）活性之间的平衡。Th1/Th2假说源于1986年的研究，该研究表明小鼠辅助性T细胞表达不同的细胞因子模式。这一假说被应用于人类免疫，Th1和Th2辅助性细胞指导不同的免疫反应途径。Th1细胞驱动1型途径（“细胞免疫”）以对抗病毒和其他细胞内病原体、消除癌细胞并刺激迟发型超敏反应（DTH）皮肤反应。Th2细胞驱动2型途径（“体液免疫”）并上调抗体产生以对抗细胞外生物体；2型优势被认为与孕期对异种移植物和胎儿的耐受性有关。任何一种模式的过度激活都可能导致疾病，并且任何一条途径都可以下调另一条途径。但该假说存在重大矛盾之处；人类细胞因子活性很少完全属于Th1或Th2模式。非辅助性调节性T细胞或抗原呈递细胞（APC）可能以与Th1和Th2细胞类似地方式影响免疫。许多先前被归类为Th1或Th2主导的疾病并不符合既定标准。在实验中，通过消耗细胞内谷胱甘肽，Th1极化很容易转变为Th2优势，反之亦然。汞会消耗谷胱甘肽并偏向Th2优势。几种营养素和激素可显著影响Th1/Th2平衡，包括植物甾醇/甾烷醇、褪黑素、益生菌、孕酮以及矿物质硒和锌。长链ω-3脂肪酸二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）可显著改善多种炎症和自身免疫性疾病，而没有任何特定的Th1/Th2效应。基于Th1/Th2的免疫疗法，例如T细胞受体（TCR）肽和白细胞介素-4（IL-4）注射，迄今为止产生了喜忧参半的结果。
