Brandtzaeg Per
Laboratory for Immunohistochemistry and Immunopathology, Department and Institute of Pathology, University of Oslo, Rikshospitalet-Radiumhospitalet Medical Center, Norway.
Ann N Y Acad Sci. 2007 Mar;1098:288-311. doi: 10.1196/annals.1384.012.
Two major antibody classes operate in saliva: secretory IgA (SIgA) and IgG. The former is synthesized as dimeric IgA by plasma cells (PCs) in salivary glands and is exported by the polymeric Ig receptor (pIgR). Most IgG in saliva is derived from serum (mainly via gingival crevices), although some is locally produced. Gut-associated lymphoid tissue (GALT) and nasopharynx-associated lymphoid tissue (NALT) do not contribute equally to mucosal PCs throughout the body. Thus, enteric immunostimulation is an inadequate mode of stimulating salivary IgA antibodies, which are poorly associated with the intestinal SIgA response, for instance after enteric cholera vaccination. Nevertheless, the IgA response in submandibular/sublingual glands is better related to B cell induction in GALT than the parotid response. Such disparity is suggested by the elevated levels of IgA in submandibular secretions of AIDS patients, paralleling their highly upregulated intestinal IgA system. Moreover, in patients with active celiac disease, IgA antibodies to disease-precipitating gliadin are reliably represented in whole saliva but not in parotid secretion. Parotid SIgA may be more consistently linked to immune induction in palatine tonsils and adenoids (human NALT), as supported by the homing molecule profile of NALT-derived B cell blasts. Also several other variables influence the levels of antibodies in oral secretions. These include difficulties with reproducibility and standardization of immunoassays, the impact of flow rate, acute or chronic stress, protein loss during sample handling, and uncontrolled admixture of serum-derived IgG and monomeric IgA. Despite such problems, saliva remains an interesting biological fluid with great scientific and clinical potentials.
分泌型IgA（SIgA）和IgG。前者由唾液腺中的浆细胞（PCs）合成为二聚体IgA，并通过聚合免疫球蛋白受体（pIgR）输出。唾液中的大多数IgG来源于血清（主要通过牙龈沟），不过也有一些是局部产生的。肠道相关淋巴组织（GALT）和鼻咽相关淋巴组织（NALT）对全身黏膜PCs的贡献并不相同。因此，肠道免疫刺激并不是刺激唾液IgA抗体的充分方式，例如在口服霍乱疫苗后，唾液IgA抗体与肠道SIgA反应的相关性较差。然而，下颌下腺/舌下腺中的IgA反应与GALT中B细胞的诱导比腮腺反应的相关性更好。艾滋病患者下颌下分泌物中IgA水平升高，与其高度上调的肠道IgA系统平行，提示了这种差异。此外，在患有活动性乳糜泻的患者中，针对致病麦醇溶蛋白的IgA抗体在全唾液中能可靠地检测到，但在腮腺分泌物中则检测不到。如NALT来源的B细胞母细胞的归巢分子谱所示，腮腺SIgA可能与腭扁桃体和腺样体（人类NALT）中的免疫诱导更一致相关。还有其他几个变量会影响口腔分泌物中的抗体水平。这些变量包括免疫测定的可重复性和标准化困难、流速的影响、急性或慢性应激、样品处理过程中的蛋白质损失以及血清来源的IgG和单体IgA的不受控制的混合。尽管存在这些问题，唾液仍然是一种具有巨大科学和临床潜力的有趣生物流体。
