Evaluation of T helper-1/-2 balance on the basis of IgG subclasses and serum cytokines in children with glomerulonephritis

Kawasaki, Yukihiko; Suzuki, Junzo; Sakai, Norisuke; Isome, Masato; Nozawa, Ruriko; Tanji, Mieko; Suzuki, Hitoshi

doi:10.1053/j.ajkd.2004.03.029

Cited by 47 publications

(44 citation statements)

References 22 publications

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“…Glomerular expression of CD40 and a high ratio of Th1/ Th2 cytokine-expressing cells in class IV proliferative lupus nephritis compared with class V lupus nephritis (101) are consistent with involvement of Th1 responses in crescentic injury. However, in children with lupus nephritis, both Th1 and Th2 antibody isotypes were observed in glomeruli (102). Expression of IL-4 and IL-10 mRNA in the absence of IFN-␥ (99) in patients with class IV lupus nephritis is consistent with a Th2 phenotype, as is expression of the CCR4 chemokine receptor on intrarenal CD4…”

Section: Lupus Nephritismentioning

confidence: 75%

T Cells in Crescentic Glomerulonephritis

Tipping

Holdsworth

2006

Journal of the American Society of Nephrology

160

150

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G lomerulonephritis (GN) is not a single disease but shows a variety of histologic patterns, clinical features, and outcomes that indicate multiple pathogenic mechanisms. A pivotal role for adaptive immune responses in initiation of GN has been demonstrated in experimental models, but across the spectrum of human GN, direct evidence of immune pathogenesis is more variable. The strongest case that adaptive immune responses drive nephritogenic events in glomeruli in humans has been mounted in crescentic GN, and evidence for involvement of autoimmunity, either organspecific autoimmunity to glomerular antigens (e.g., anti-glomerular basement membrane [anti-GBM] GN) or systemic autoimmunity to nonglomerular antigens (e.g., ANCA-associated crescentic GN, lupus nephritis) now is emerging for many forms of human crescentic GN. CD4 ϩ T cells play a central role in adaptive immunity. T cell-independent responses are uncommon. They usually are associated with simple carbohydrate-rich antigens and do not show extensive Ig isotype switching or strong affinity maturation. The known antigens that drive crescentic GN show strong evidence of CD4 ϩ T cell dependence and do not have the characteristics of T-independent antigens. The evidence from glomerular pathology also suggests a prominent role for local CD4 ϩ T cell-driven Th1-type responses in crescentic GN with delayed-type hypersensitivity (DTH)-like cellular effectors (T cells and macrophages) as well as Th1 Ig isotypes in glomeruli.The relative contributions of cellular and humoral CD4 ϩ T cell-driven effectors, particularly in ANCA-associated GN, remains controversial, but it is clear that the nephritogenic immune responses are CD4 ϩ T cell-driven.

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Section: Lupus Nephritismentioning

confidence: 75%

T Cells in Crescentic Glomerulonephritis

Tipping

Holdsworth

2006

Journal of the American Society of Nephrology

160

150

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“…Other authors have confirmed the proliferative LN Th1 dominance in humans [114, 115]. However, in pediatric LN, a balance between Th1/Th2 on the basis of IgG subclasses has been detected [118, 119]. In proliferative LN, there is overexpression of TNF-related apoptosis-inducing ligand (TRAIL) in the glomerular tubules of patients [120].…”

Section: Pathogenesis and Antibodiesmentioning

confidence: 99%

Lupus Nephritis: An Overview of Recent Findings

Salgado

Herrera-Diaz

2012

Autoimmune Diseases

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Lupus nephritis (LN) is one of the most serious complications of systemic lupus erythematosus (SLE) since it is the major predictor of poor prognosis. In susceptible individuals suffering of SLE, in situ formation and deposit of immune complexes (ICs) from apoptotic bodies occur in the kidneys as a result of an amplified epitope immunological response. IC glomerular deposits generate release of proinflammatory cytokines and cell adhesion molecules causing inflammation. This leads to monocytes and polymorphonuclear cells chemotaxis. Subsequent release of proteases generates endothelial injury and mesangial proliferation. Presence of ICs promotes adaptive immune response and causes dendritic cells to release type I interferon. This induces maturation and activation of infiltrating T cells, and amplification of Th2, Th1 and Th17 lymphocytes. Each of them, amplify B cells and activates macrophages to release more proinflammatory molecules, generating effector cells that cannot be modulated promoting kidney epithelial proliferation and fibrosis. Herein immunopathological findings of LN are reviewed.

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“…In humans, immunity driven by T‐helper 1 cytokines is required for protection from Staphylococcus spp. infection, whereas these cytokines promote inflammation in Malassezia spp. infections .…”

Section: Discussionmentioning

confidence: 99%

Antibody levels to Malassezia pachydermatis and Staphylococcus pseudintermedius in atopic dogs and their relationship with lesion scores

Khantavee

Chanthick

Sookrung

et al. 2019

Veterinary Dermatology

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Background Elevated immunoglobulin E (IgE) levels to Malassezia or Staphylococcus species in human atopic dermatitis are related to the skin severity index; a similar association has not been reported in atopic dogs. Objectives To investigate serum levels of allergen‐specific IgE, total specific IgG and IgG subclasses (IgG1 and IgG2) for M. pachydermatis and S. pseudintermedius, and to correlate them with the severity of dermatitis in dogs. Animals Serum samples were collected from dogs categorized by age and disease status. Groups 1 and 2: <3‐year‐old healthy (n = 9) and atopic dogs (n = 9), respectively; and groups 3 and 4: ≥3‐year‐old healthy (n = 11) and atopic dogs (n = 14), respectively. Methods and materials Antibody levels were measured by ELISA. The Canine Atopic Dermatitis Lesion Index (CADLI) was analyzed in relation to antibody levels. Results Specific IgE and total IgG against M. pachydermatis and S. pseudintermedius were significantly increased in atopic dogs of all ages. Although differences between atopic and healthy dogs, with regard to specific IgG1 and IgG2 levels to each microbe, varied in significance within age groups. No significant relationships were found between the CADLI and any specific immunoglobulin levels for both microbe types. Conclusions and clinical importance In dog skin, microbes may act as allergens triggering inflammatory responses via IgE‐ and IgG‐dependent pathway(s). The affinity of the IgG subclass produced may vary according to antigen type. Specific IgE levels may be related to clinical disease in dogs and not to skin lesion severity.

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Evaluation of T helper-1/-2 balance on the basis of IgG subclasses and serum cytokines in children with glomerulonephritis

Cited by 47 publications

References 22 publications

T Cells in Crescentic Glomerulonephritis

T Cells in Crescentic Glomerulonephritis

Lupus Nephritis: An Overview of Recent Findings

Antibody levels to Malassezia pachydermatis and Staphylococcus pseudintermedius in atopic dogs and their relationship with lesion scores

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