scholarly journals Microbial IgA Protease Removes IgA Immune Complexes from Mouse Glomeruli In Vivo: Potential Therapy for IgA Nephropathy

2008 ◽  
Vol 172 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Michael E. Lamm ◽  
Steven N. Emancipator ◽  
Janet K. Robinson ◽  
Michifumi Yamashita ◽  
Hisashi Fujioka ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Iga Immune Complexes ◽  
Iga Protease

scholarly journals Experimental IgA nephropathy.

1979 ◽  
Vol 150 (5) ◽  
pp. 1161-1173 ◽  
Author(s):  
A Rifai ◽  
P A Small ◽  
P O Teague ◽  
E M Ayoub
Keyword(s):  
Iga Nephropathy ◽  
Immune Complex ◽  
Immune Complexes ◽  
Secretory Iga ◽  
Glomerular Lesions ◽  
Glomerular Deposits ◽  
Focal Glomerulonephritis ◽  
Iga Immune Complexes

An animal model for IgA immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma, and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar, but more severe pathological changes were produced with complexes formed in vivo either in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings as well as the distribution of the immune complexes within the affected glomeruli, are some of the features which bear resemblance between this experimental model and human IgA nephropathy. Fixation of complements by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, was shown to occur in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 glomerular deposits was similar to that of IgA. However, complement proved to be nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was observed to be critical for renal deposition of complexes and induction of nephritic histological changes. In contrast, monomeric IgA immune complexes failed to produce glomerular deposits. This finding raises the possibility that secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.

scholarly journals Bacterial IgA protease-mediated degradation of agIgA1 and agIgA1 immune complexes as a potential therapy for IgA Nephropathy

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Li Wang ◽  
Xueying Li ◽  
Hongchun Shen ◽  
Nan Mao ◽  
Honglian Wang ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Iga Protease

Detection of bovine serum albumin in the circulating IgA immune complexes of patients with IgA nephropathy

1987 ◽  
Vol 43 (3) ◽  
pp. 395-402 ◽  
Author(s):  
Hui Kim Yap ◽  
Rebecca S. Sakai ◽  
Keng Thye Woo ◽  
Cheng Hong Lim ◽  
Stanley C. Jordan
Keyword(s):  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Iga Nephropathy ◽  
Immune Complexes ◽  
Bovine Serum ◽  
Iga Immune Complexes

Levels of Circulating IgA Immune Complexes after Gluten-Rich Diet in Patients with IgA Nephropathy

Nephron ◽  
1988 ◽  
Vol 49 (2) ◽  
pp. 104-106 ◽  
Author(s):  
Mitsunori Yagame ◽  
Yasuhiko Tomino ◽  
Kazuhiko Eguchi ◽  
Masahiko Miura ◽  
Takao Suga ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Iga Immune Complexes

scholarly journals IgA Glycosylation and IgA Immune Complexes in the Pathogenesis of IgA Nephropathy

2008 ◽  
Vol 28 (1) ◽  
pp. 78-87 ◽  
Author(s):  
Jan Novak ◽  
Bruce A. Julian ◽  
Milan Tomana ◽  
Jiri Mestecky
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Iga Immune Complexes

scholarly journals Pathogenesis of IgA Nephropathy: Current Understanding and Implications for Development of Disease-Specific Treatment

2021 ◽  
Vol 10 (19) ◽  
pp. 4501
Author(s):  
Barbora Knoppova ◽  
Colin Reily ◽  
R. Glenn King ◽  
Bruce A. Julian ◽  
Jan Novak ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Mesangial Cells ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Pathogenic Potential ◽  
Clinical Observations ◽  
Circulating Levels ◽  
Disease Specific

IgA nephropathy, initially described in 1968 as a kidney disease with glomerular “intercapillary deposits of IgA-IgG”, has no disease-specific treatment and is a common cause of kidney failure. Clinical observations and laboratory analyses suggest that IgA nephropathy is an autoimmune disease wherein the kidneys are damaged as innocent bystanders due to deposition of IgA1-IgG immune complexes from the circulation. A multi-hit hypothesis for the pathogenesis of IgA nephropathy describes four sequential steps in disease development. Specifically, patients with IgA nephropathy have elevated circulating levels of IgA1 with some O-glycans deficient in galactose (galactose-deficient IgA1) and these IgA1 glycoforms are recognized as autoantigens by unique IgG autoantibodies, resulting in formation of circulating immune complexes, some of which deposit in glomeruli and activate mesangial cells to induce kidney injury. This proposed mechanism is supported by observations that (i) glomerular immunodeposits in patients with IgA nephropathy are enriched for galactose-deficient IgA1 glycoforms and the corresponding IgG autoantibodies; (ii) circulatory levels of galactose-deficient IgA1 and IgG autoantibodies predict disease progression; and (iii) pathogenic potential of galactose-deficient IgA1 and IgG autoantibodies was demonstrated in vivo. Thus, a better understanding of the structure–function of these immunoglobulins as autoantibodies and autoantigens will enable development of disease-specific treatments.

Presence of Specific IgA Immune Complexes in IgA Nephropathy

2015 ◽  
pp. 80-86 ◽  
Author(s):  
J. Egido ◽  
J. Sancho ◽  
P. Hernando ◽  
J. Gonz�lez ◽  
L. Hernando
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Iga Immune Complexes

Detection of Circulating Immune Complexes in the Sera of Rabbits with Experimental Syphilis: Possible Role in Immunoregulation

1980 ◽  
Vol 29 (2) ◽  
pp. 575-582
Author(s):  
Robert E. Baughn ◽  
Kenneth S. K. Tung ◽  
Daniel M. Musher
Keyword(s):  
Immune Complexes ◽  
Proteolytic Enzymes ◽  
Suppressor Cell ◽  
Suppressive Effect ◽  
Circulating Immune Complexes ◽  
Time Period ◽  
Infected Cells ◽  
Disseminated Disease

The in vivo and in vitro immunoglobulin G plaque-forming cell responses to sheep erythrocytes (SRBC) are nearly obliterated during disseminated syphilitic infection (3 to 8 weeks post-intravenous injection) in rabbits. Splenic and lymph node cells obtained from infected rabbits during this time period were capable of suppressing the normal in vitro responses of uninfected, SRBC-primed cells. Cell-free washings of cells from infected animals were also suppressive. This finding coupled with the fact that treatment of infected cells with proteolytic enzymes abrogated the suppressive effect constitute arguments against involvement of a specific suppressor cell population. The incidence of elevated levels of circulating immune complexes in the sera of rabbits with disseminated disease was also significantly different from that of uninfected controls or infected rabbits before the onset or after the regression of lesions. When added to cultures of lymphocytes from uninfected, SRBC-sensitized rabbits, sera containing complexes caused dose-related suppression of the in vitro immunoglobulin responses. Unlike immune complexes, no correlation was found between the presence of mucopolysaccharide materials and the stage of infection or the ability of serum to suppress the immunoglobulin responses to SRBC.

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