“…3 (33) at similar concentrations as in other mammals (2), but large additional amounts of m-IgA, not found in most mammals (34) make it the minor component of IgA in human serum. The higher proportions of plasma cells staining for p-IgA (35,36) or for IgA2 (37) in mucosae than in bone marrow (35,38), and the higher proportions of p-IgA (1, 2) or of IgA2 (6, 7) in secretions than in serum, led some authors to regard serum p-IgA and/or IgA2 as being mainly of mucosal origin (2,10,13). In contrast, mIgA and IgAl in serum are likely to originate predominantly from bone marrow (39) where IgAl plasmacytes predominate and are the largest producers of m-IgA in vitro (40).…”
Section: Resultsmentioning
confidence: 99%
“…IJBP, ileojejunal bypass; IRMA, immunoradiometric assay; LD, liver disease(s); m-IgA, monomeric IgA; PBC, primary biliary cirrhosis; PBS, phosphatebuffered saline; p-IgA, polymeric IgA; RA, rheumatoid arthritis; SC, secretory component; SDGU, sucrose density gradient ultracentrifugation; sIgA, secretory IgA; SLE, systemic lupus erythematosus. p-IgA was found (1,10,11), whereas conflicting results regarding serum p-IgA in Berger's disease exist (12)(13)(14). Some experimental (15) and clinical evidence (16,17) suggests that p-IgA may be directly involved in tissue injury in some diseases.…”
Section: Introductionmentioning
confidence: 99%
“…Some experimental (15) and clinical evidence (16,17) suggests that p-IgA may be directly involved in tissue injury in some diseases. Changes in subclass proportions in pathological sera have not been studied but there are conflicting data about the IgA subclass deposits in Berger's disease (13,18,19).…”
A B ST R A CT We have studied the relative contributions of monomeric (m-) and polymeric IgA (p-IgA) and of IgAl and IgA2 to total serum IgA in healthy adults and patients with liver disease (LD) or with other diseases and high serum IgA. Serum concentration of total secretory component (SC) was also determined. In addition, fractional catabolic rates (FCR) and synthetic rates for both m-and p-IgA were measured in nine controls and nine cirrhotics. Our results support four main conclusions: (a) In healthy adults, intravascular p-IgA contributes to only 4-22% (mean 12%) of serum IgA, because its FCR and synthetic rate are approximately two times higher and four times smaller, respectively, than those of intravascular mIgA. (b) In LD, biliary obstruction does not result in a significant increase in serum p-IgA unlike in rats and rabbits, indicating that in humans the SC-dependent biliary transport of p-IgA plays a much less significant role in selective removal of p-IgA from plasma than in rats and rabbits. (c) In contrast to biliary obstruction, parenchymal LD results in a significant and preferential increase in serum p-IgA, which in cirrhotics correlates with a selective reduction of the p-IgA-FCR. This supports a role for the human liver in selective removal of p-IgA from plasma, but another mechanism than the SC-dependent biliary transport should be considered. (d) Total SC, p-IgA, and IgA2 in serum are unlinked parameters, not necessarily reflecting mucosal events. A marked increase in serum SC occurs Address reprint requests to Dr. Delacroix, ICP-MEXP, Brussels, Belgium.
“…3 (33) at similar concentrations as in other mammals (2), but large additional amounts of m-IgA, not found in most mammals (34) make it the minor component of IgA in human serum. The higher proportions of plasma cells staining for p-IgA (35,36) or for IgA2 (37) in mucosae than in bone marrow (35,38), and the higher proportions of p-IgA (1, 2) or of IgA2 (6, 7) in secretions than in serum, led some authors to regard serum p-IgA and/or IgA2 as being mainly of mucosal origin (2,10,13). In contrast, mIgA and IgAl in serum are likely to originate predominantly from bone marrow (39) where IgAl plasmacytes predominate and are the largest producers of m-IgA in vitro (40).…”
Section: Resultsmentioning
confidence: 99%
“…IJBP, ileojejunal bypass; IRMA, immunoradiometric assay; LD, liver disease(s); m-IgA, monomeric IgA; PBC, primary biliary cirrhosis; PBS, phosphatebuffered saline; p-IgA, polymeric IgA; RA, rheumatoid arthritis; SC, secretory component; SDGU, sucrose density gradient ultracentrifugation; sIgA, secretory IgA; SLE, systemic lupus erythematosus. p-IgA was found (1,10,11), whereas conflicting results regarding serum p-IgA in Berger's disease exist (12)(13)(14). Some experimental (15) and clinical evidence (16,17) suggests that p-IgA may be directly involved in tissue injury in some diseases.…”
Section: Introductionmentioning
confidence: 99%
“…Some experimental (15) and clinical evidence (16,17) suggests that p-IgA may be directly involved in tissue injury in some diseases. Changes in subclass proportions in pathological sera have not been studied but there are conflicting data about the IgA subclass deposits in Berger's disease (13,18,19).…”
A B ST R A CT We have studied the relative contributions of monomeric (m-) and polymeric IgA (p-IgA) and of IgAl and IgA2 to total serum IgA in healthy adults and patients with liver disease (LD) or with other diseases and high serum IgA. Serum concentration of total secretory component (SC) was also determined. In addition, fractional catabolic rates (FCR) and synthetic rates for both m-and p-IgA were measured in nine controls and nine cirrhotics. Our results support four main conclusions: (a) In healthy adults, intravascular p-IgA contributes to only 4-22% (mean 12%) of serum IgA, because its FCR and synthetic rate are approximately two times higher and four times smaller, respectively, than those of intravascular mIgA. (b) In LD, biliary obstruction does not result in a significant increase in serum p-IgA unlike in rats and rabbits, indicating that in humans the SC-dependent biliary transport of p-IgA plays a much less significant role in selective removal of p-IgA from plasma than in rats and rabbits. (c) In contrast to biliary obstruction, parenchymal LD results in a significant and preferential increase in serum p-IgA, which in cirrhotics correlates with a selective reduction of the p-IgA-FCR. This supports a role for the human liver in selective removal of p-IgA from plasma, but another mechanism than the SC-dependent biliary transport should be considered. (d) Total SC, p-IgA, and IgA2 in serum are unlinked parameters, not necessarily reflecting mucosal events. A marked increase in serum SC occurs Address reprint requests to Dr. Delacroix, ICP-MEXP, Brussels, Belgium.
“…18,19 Certain observations suggest IgA nephropathy is associated with abnormalities of IgA regulation. IgA derived from mesangial deposits has been shown to be remarkably homogenous in anionic charge, which may be related to its affinity for the mesangium, 20,21 IgA may be deposited in the mesangium because some of its physicochemical properties trap it there, bound to deposited antigen or to intrinsic mesangial antigen, or because it has structural abnormalities.…”
Section: Disturbances In Iga Regulationmentioning
confidence: 99%
“…21 More recent studies, however, have shown that the IgA1 subclass is deposited selectively in the mesangium. [22][23][24][25] Structural abnormalities of the IgA1 may play a role in its mesangial deposition, IgA1 is one of the 2 immunoglobulin subclasses (the other is IgD) that is O-glycosylated on a number of asparagine, serine, and threonine residues in a special proline-rich hinge region.…”
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