Cell-mediated immunity in renal disease

McCluskey, Robert T.; Bhan, Atul K.

doi:10.1016/s0046-8177(86)80287-8

Cited by 17 publications

(4 citation statements)

References 61 publications

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“…A comparable pat tern was mentioned by McCluskey and Bhan [39] in druginduced acute interstitial nephritis. Willemze et al [40] demonstrated a similar ratio of T cell subsets in cuta neous mononuclear cell infiltrations of patients with con tact dermatitis which is considered a typical example of type IV (delayed-type hypersensitivity) reaction.…”

Section: Discussionsupporting

confidence: 82%

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis

Wilmink

et al. 1985

Am J Nephrol

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Clinical and immunological data are reported of 12 patients suffering from Wegener’s granulomatosis and severe renal involvement. Although 9 patients recovered from their acute illness, at long-term follow-up a relapse occurred in 4 of these 9 patients. Therefore, lifelong follow-up in this group of patients seems to be mandatory. Extensive immunological investigations did not provide evidence for humoral mechanisms underlying the pathogenesis of this disease; T lymphocyte subsets in peripheral blood as well as functional reactivity of lymphocytes in vitro were also normal. However, none of the patients was able to mount a primary cellular immune response in vivo. On the other hand, kidney biopsy specimens obtained before the initiation of drug therapy revealed periglomerular and interstitial cellular infiltrations consisting predominantly of T lymphocytes with a ratio Leu 3a (OKT4)/Leu 2a (OKT8) of 5:1. This may indicate that a type IV (delayed-type) hypersensitivity reaction takes place in the kidney. These findings suggest that an abnormal cellular immunoreactivity plays a major role in the pathogenesis of Wegener’s granulomatosis.

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Section: Discussionsupporting

confidence: 82%

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis

Wilmink

et al. 1985

Am J Nephrol

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“…In more than half of our cases with 11, no Tl D deposits were detected confirming the findings of others [7], This discrepancy can be explained in several ways: (1) TID may disappear more rapidly than the cellular inflamma tion they bring about; (2) the membrane attack complex of the complement system (C5-C9), demonstrated in the tubulointerstitial tissue often in the absence of immunog lobulins or early complement fractions, may cause cellu lar damage leading to a secondary inflammatory re sponse [5]; (3) cell-mediated immunity may be operative [41,42]; (4) inflammatory cells may drain from glomeruli with active lesions into the interstitium through the mes angial-juxtaglomerular axis, as suggested by the frequent finding of interstitial inflammatory cells predominantly around glomeruli, especially at the vascular pole (fig. 8); and (5).…”

Section: Discussionmentioning

confidence: 99%

Tubulointerstitial Disease in Lupus Nephritis: Relationship to Immune Deposits, Interstitial Inflammation, Glomerular Changes, Renal Function, and Prognosis

Park¹,

D’Agati²,

Appel

et al. 1986

Nephron

126

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The interrelationships between tubulointerstitial immune deposits (TID), interstitial inflammation, glomerular changes, renal function, and prognosis were assessed in the renal biopsies from 93 patients with lupus nephritis. The prevalence of TID was 33% by immunofluorescence and 23% by electron microscopy. Although predominantly detected along and within tubular basement membranes, extraglomerular immune deposits were also present in the wall of renal interstitial capillaries and small arteries as well as in Bowman’s capsule. The prevalence of TID correlated with the activity of glomerular lesions and, to a lesser extent, with the severity of proliferative lupus nephritis (WHO classes II-IV).TID were much less common in the membranous form (WHO class V). The severity of interstitial inflammation correlated with the degree of renal insufficiency and was an accurate prognostic indicator of progressive deterioration of renal function. However, there was no correlation between prevalence of TID and prevalence and severity of interstitial inflammation, suggesting that the latter is not necessarily secondary to the presence of immune complexes and that other pathogenetic mechanisms may be involved.

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“…In WG, granulomatous reactions occur, possibly as the result of sensitized T lymphocytes reacting with antigen and releasing various cytokines that recruit macrophages to the site of injury. The activated macrophages release lysosomal enzymes and cause local tissue injury [9,13]. The most commonly cited hypothesis for the role of ANCA in the pathogenesis of vascular injury is that an undetermined stimulus, perhaps an infection, elicits inflammatory cytokines that induce the expression of ANCA target antigens (proteinase 3 and/or myeloperoxidase) on the neutrophil cell surface.…”

Section: Discussionmentioning

confidence: 99%

A boy with consecutive development of SLE and Wegener granulomatosis

Erdoğan

Öner

Demircin

et al. 2004

Pediatric Nephrology

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An 11-year-old boy with consecutive development of systemic lupus erythematosus (SLE) and Wegener granulomatosis (WG) is presented. He was first admitted to the hospital with the findings of SLE, including crescentic glomerulonephritis, Coombs' test-positive hemolytic anemia, hypocomplementemia, antinuclear antibody (ANA) positivity, and elevated levels of anti-double-stranded (ds) DNA antibodies. He was treated successfully with steroids, cyclophosphamide, and peritoneal dialysis. One month after his discharge he developed an apparent viral infection. Three weeks afterwards he was readmitted with the findings of lower respiratory tract involvement, maxillary sinusitis, nasal septum perforation, p- and c-antineutrophil cytoplasmic antibody (ANCA) positivity, but normal complement, ANA, and anti-ds DNA levels, suggesting the diagnosis of WG. He did not respond to anti-infectious and immunosuppressive treatment, and he died of Pseudomonas sepsis.

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Cell-mediated immunity in renal disease

Cited by 17 publications

References 61 publications

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis

Tubulointerstitial Disease in Lupus Nephritis: Relationship to Immune Deposits, Interstitial Inflammation, Glomerular Changes, Renal Function, and Prognosis

A boy with consecutive development of SLE and Wegener granulomatosis

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Cell-mediated immunity in renal disease

Cited by 17 publications

References 61 publications

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener&rsquo;s Granulomatosis

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener&rsquo;s Granulomatosis

Tubulointerstitial Disease in Lupus Nephritis: Relationship to Immune Deposits, Interstitial Inflammation, Glomerular Changes, Renal Function, and Prognosis

A boy with consecutive development of SLE and Wegener granulomatosis

Contact Info

Product

Resources

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Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis

Clinical and Immunological Follow-Up of Patients with Severe Renal Disease in Wegener’s Granulomatosis