Evidence for Migration of IgA Bearing Lymphocytes between Peripheral Muscosal Sites

Human IgA inhibits adherence ofAcanthamoeba polyphagato epithelial cells and contact lenses

“…Although IgA antibodies against Acanthamoeba in saliva and colostrum may not directly participate in the resistance to amoebic invasion, IgA-containing lymphocytes in the mammary gland (Montgomery et al 1985) and other sites of the mucosal-associated lymphoid tissue can migrate into the lacrimal gland (Montgomery et al 1983;Sullivan 1999). In tears, the secretory IgA antibodies may avoid corneal infections, since adhesion of A. polyphaga to contact lenses (Towbin et al 1979;Sharma et al 1995) and epithelial cells Khan 2001) plays an important role in the pathogenesis of Acanthamoeba keratitis.…”

Ocular Mucosal Immunity

“…In some animal species, components of CALT were described in conjunctiva, showing species-specific differences (Axelrod and Chandler, 1979;Franklin and Remus, Rat l IgA (predominant), IgG (IgG1, IgG2a, IgG2b, IgG2c) and IgM plasma cells l Surface IgM-, IgA-, and IgG-bearing B cells l Macrophages, mast cells l Recent thymic emigrants; CD8 + and CD4 + , effector, naïve and memory (rare) T cells; αEβ7 + T cells; natural killer T cells; and possibly extrathymic T cells l Mast cells Ebersole et al (1988), Gudmundsson et al (1985), Allansmith et al (1987), Hann et al (1988), Pappo et al (1988), Montgomery et al (1990), Sullivan et al (1990c, Williams et al (1994), O 'Sullivan et al (1998'Sullivan et al ( , 2001, Sullivan et al (1998), andSchechter et al (2010) Mouse l IgA (predominant), IgG, and IgM plasma cells l Surface IgA-, IgG-, or IgM-bearing B cells l Natural killer T cells, B1 cells l Mast cells l Th17, Treg McGee and Franklin (1984), Montgomery et al (1985), Saitoh-Inagawa et al (2000), Chauhan et al (2009), andSchechter et al (2010) Ig, immunoglobulin; Treg, regulatory T cell; HML-1, human mucosal lymphocyte-1 antigen.…”

“…Remote-site stimulation would most likely involve IgA lymphoblast migration from nasal-or gastrointestinal-associated lymphoid tissue, and from cervical or mesenteric lymph nodes, via the thoracic duct lymph, to the lacrimal gland (Montgomery et al, 1983(Montgomery et al, , 1985McGee and Franklin, 1984;O'Sullivan and Montgomery, 1990;Montgomery and Whittum-Hudson, 1996), followed by local antibody production and transport to the ocular surface. In contrast, the contribution of serum IgA antibodies to ocular surface defense appears to be minimal or nonexistent (Sullivan and Allansmith, 1984;Montgomery et al, 1984b;Bergmann et al, 1986;Peppard and Montgomery, 1987;Czerkinsky et al, 1987).…”

Local Immune Responses in Ocular Virus Infection and Their Implications for Future Immunotherapy

“…Ocular viral antigens are pro cessed in the submandibular, cervical or preauricular lymph nodes. They are trapped in the nasal, oral or gut epithelium and stimulate peripheral mesenteric, gut-asso ciated, mammary gland and/or splenic lymphocytes [61,62], These committed lymphocytes migrate through the peripheral blood system and home in on the lacrimal glands, CALT, cornea and other inflammatory sites [63]. Consistent with this pattern, when the virus-infected mu cosal membrane is in a remote site or viral vaccine is administered via an intranasal, oral, gastric or vaginal route, specific tear IgA antibody increases and generates ocular surface protection [64,65], Anti-viral IgG and IgM also increase in the tear film.…”