Brandtzaeg P, Valnes K, Scott H, Rognum T O, Bjerke K, Baklien K
Scand J Gastroenterol Suppl. 1985;114:17-38. doi: 10.3109/00365528509093765.
The main function of secretory IgA is to exert immune exclusion; that is, by intimate cooperation with innate non-specific defence mechanisms, it dampens down penetration of soluble antigens and inhibits epithelial colonisation of bacteria and viruses. Secretory IgM may exert a similar protective function in the gut as its local synthesis sometimes is markedly increased, especially in selective IgA deficiency. IgG should not be considered a secretory immunoglobulin because its external translocation depends on passive intercellular diffusion. By activating complement, antibodies of this isotype may cause increased mucosal permeability and tissue damage. IgG may thus contribute to persistent immunopathology in mucosal lesions. The same is true for IgE antibodies which, in atopic individuals, may be carried into the gut mucosa by mast cells and cause their degranulation with histamine release. Secretory IgA and secretory IgM are the products of two cell types: plasma cells synthesise IgA dimers and IgM pentamers which, by non-covalent association, become complexed with the secretory component (SC) which is synthesized by serous-type glandular cells. The adsorption of the Ig polymers to the SC-expressing epithelial cells depends on J chain-determined binding sites. This fact gives biological significance to the striking J chain expression shown by mucosal immunocytes regardless of the Ig class they produce. The immunocytes populating the gut mucosa apparently belong to relatively early memory B cell clones. The obvious functional goal of J chain expression at this stage of clonal differentiation is local generation of SC-binding IgA and IgM polymers. In various gut diseases, altered immune regulation results in a disproportionately increased number of J chain-negative IgG-producing cells in the mucosa. Such altered immunological homeostasis may contribute to perpetuation of inflammatory bowel diseases.
分泌型IgA的主要功能是发挥免疫排除作用；也就是说，通过与先天性非特异性防御机制密切协作，它可减少可溶性抗原的穿透，并抑制细菌和病毒在上皮的定植。分泌型IgM在肠道中可能发挥类似的保护作用，因为其局部合成有时会显著增加，尤其是在选择性IgA缺乏的情况下。IgG不应被视为分泌型免疫球蛋白，因为其向外转运依赖于被动的细胞间扩散。通过激活补体，该同种型抗体可能会导致黏膜通透性增加和组织损伤。因此，IgG可能会导致黏膜病变中持续性免疫病理状态。IgE抗体也是如此，在特应性个体中，它们可能由肥大细胞带入肠道黏膜，并导致其脱颗粒并释放组胺。分泌型IgA和分泌型IgM是两种细胞类型的产物：浆细胞合成IgA二聚体和IgM五聚体，它们通过非共价结合与由浆液性腺细胞合成的分泌成分（SC）形成复合物。Ig聚合物与表达SC的上皮细胞的吸附取决于J链决定的结合位点。这一事实赋予了黏膜免疫细胞显著的J链表达生物学意义，而不论它们产生何种Ig类别。定居于肠道黏膜的免疫细胞显然属于相对早期的记忆B细胞克隆。在克隆分化的这个阶段，J链表达的明显功能目标是在局部产生与SC结合的IgA和IgM聚合物。在各种肠道疾病中，免疫调节改变导致黏膜中产生J链阴性IgG的细胞数量不成比例地增加。这种免疫稳态的改变可能会导致炎症性肠病持续存在。
