Rat Monocytes in a Model of Combined Injury Express the OX8 Antigen

Kaffenberger, W.; Gruber, Dale F.; MacVittie, T J

doi:10.1002/jlb.42.3.181

Cited by 9 publications

(8 citation statements)

References 8 publications

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“…Whether the b-chain was also present could not be assessed as MoAb 341 gave equivocal staining results. There is increasing evidence that CD8 may occur in cells other than T cells and NK cells, and a population of Ox8-positive monocytes has been detected by flow cytometry in a rat model of sublethal total-body irradiation followed by thermal injury [55]. In addition, rat Kupffer cell precursors [51], a subpopulation of tumour-infiltrating dendritic cells in rats [56], certain dendritic cells in the thymus and spleen of normal mice [57,58] and peritoneal as well as alveolar macrophages [59] express the CD8 antigen.…”

Section: Discussionmentioning

confidence: 99%

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

Scriba

Steiniger

1998

Scand J Immunol

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Scriba A, Grau V, Steiniger B. Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR-P1 and Reduction of CD43. Scand J Immunol 1998;47;332-342 Monocytes and macrophages mediate cytotoxicity after appropriate activation and thus represent effectors secondary to T lymphocytes and natural killer (NK) cells. However, very little is known about the role of activated monocytes in organ allograft rejection. In this study, isogeneic (LEW to LEW) and fully allogeneic (DA to LEW) rat kidneys were grafted to bilaterally nephrectomized recipients. Four days after transplantation a comprehensive sample of leucocytes was recovered by perfusion of the recipients' vasculature with phosphate-buffered saline containing EDTA (PBS/EDTA). Monocytes were enriched by density gradient centrifugation and their physical parameters and immunophenotype were investigated by flow cytometry in comparison with untreated, specified pathogen-free (SPF) LEW rats. Isotransplantation and allotransplantation of kidneys dramatically increased the absolute number of intravascular monocytes in the recipient. Analysis of NKR-P1 (CD161), CD4, CD62L, CD43, CD11a, CD18 and MHC class II expression identified at least two monocyte populations in all experimental groups. In graft recipients it was evident that activated monocytes were able to express and upregulate NKR-P1 and CD8, which have not been detected in these cells to date. If activated monocytes utilize NKR-P1 and CD8, by analogy to NK cells and lymphocytes these cells may be endowed with additional pathways to upregulate cytolytic functions and effect allograft damage. Professor B. Steiniger,

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Section: Discussionmentioning

confidence: 99%

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

Scriba

Steiniger

1998

Scand J Immunol

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“…Current evidence suggests that CD8␣ protein is expressed by NK cells in rat [27] and human [28] but not in mouse [29] ( Table 1 and references therein). Similarly rat [42,44] and human monocytes [31] and macrophages [35] express CD8␣, and the same cells in the mouse lack CD8␣ [33]. Intriguingly, rat macrophages and mast cells also express CD8␤ [35,36].…”

Section: Cell Types That Express Cd8 and Cd4 Vary Among Mammalian Spementioning

confidence: 99%

“…Large numbers of CD8 ϩ macrophages and monocytes have been observed in several models of disease in rats, including glomerulonephritis [102], arthritis [103], ischemia [104], severe trauma [44], transplant rejection [42], experimental allergic encephalomyelitis [105], autoimmune thyroid disease [106], myocarditis [5], viral infection [107], and tumors [3]. CD8 ϩ monocytes increase proportionally after induction of several of these diseases, express markers associated with cytotoxicity [5], and localize to sites of tissue destruction [102], suggesting that they may have an active role in causing tissue pathology.…”

Section: A Role For Cd8 In Cytotoxic Responses Of Monocytes and Macromentioning

confidence: 99%

CD4 and CD8: an inside-out coreceptor model for innate immune cells

Gibbings

Befus

2009

Journal of Leukocyte Biology

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CD8 and CD4 are expressed by several cell types that do not express TCR. These include DCs, macrophages, monocytes, and NK cells. CD8(+) monocytes and macrophages are abundant at the site of pathology in many rat disease models, particularly those involving immune complex-mediated pathology. Indeed, in some disease models, CD8(+) macrophages correlate with severity of pathology or directly cause pathology or tumor cell killing. Evidence suggests CD8 or CD4 can enhance FcgammaR-dependent responses of human monocytes. Building on data that key components of TCR and FcgammaR signaling can substitute one another efficiently, we postulate that CD4 and CD8 operate with FcgammaR and potentially other receptors to enhance responses of T cells and various innate immune cells. Our model suggests CD8 on myeloid cells may contribute directly to tumor killing and tissue pathology by enhancing FcgammaR responses. Moreover, the model suggests a role for CD8 in cross-presentation of antibody-associated antigen by DCs and a new mechanism to regulate TCR sensitivity.

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“…1 It has been reported that monocytes may be induced to express OX8 in vivo [24]. In our laboratory, lymphocyte-depletion studies with monoclonal antibody OX8 given intraperitoneally resulted in a significant reduction in circulating monocyte numbers [unpubl.…”

Section: Renal Immunofluorescence Studiesmentioning

confidence: 99%

“…The pattern of reactivity of these antibodies is summarized in table I [for a more detailed discussion, see ref. [18][19][20]24].…”

Section: Characterization O F Interstitial Cellsmentioning

confidence: 99%

Tubuloînterstitial Nephritis during the Heterologous Phase of Nephrotoxic Serum Nephritis

Eddy

1991

Nephron

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This study was designed to characterize the immunopathology of acute tubuloînterstitial disease in nephrotoxic serum nephritis in nonsensitized rats. Groups of Lewis rats were studied at 12 time periods ranging from 10 min to 28 days after nephrotoxic serum injection. Nephritic rats developed interstitial nephritis during the acute heterologous phase of renal injury. Coincident with the focal deposition of nephrotoxic antibodies along tubular basement membranes at 24 h, an influx of polymorphonuclear cells and macrophages was evident. The most prominent infiltrate, present between days 3 and 7, was dominated by macrophages with smaller numbers of lymphocytes that were mainly cytotoxic T cells. Dual-labeling studies demonstrated the colocalization of linear tubular basement membrane deposits of the nephrotoxic antibody with focal clusters of interstitial lymphohemopoietic cells. Increased complement deposition was not evident along the tubular basement membranes; moreover, C3 depletion with cobra venom factor failed to attenuate the interstitial inflammation. During the late autologous phase of glomerulonephritis, tubular basement membrane deposits of rat IgG did not appear and the interstitial disease resolved. The results of this study demonstrate that the heterologous phase of nephrotoxic serum nephritis is an antibody-mediated disease directed against the basement membranes not only of the glomeruli but also of some tubules. Antibody deposition is followed by an acute influx of phagocytic cells to both regions of the kidney. These cells may play an important role in the genesis of acute interstitial injury and chronic interstitial fibrosis associated with antiglomerular basement membrane nephritis.

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Rat Monocytes in a Model of Combined Injury Express the OX8 Antigen

Cited by 9 publications

References 8 publications

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

Phenotype of Rat Monocytes During Acute Kidney Allograft Rejection: Increased Expression of NKR‐P1 and Reduction of CD43

CD4 and CD8: an inside-out coreceptor model for innate immune cells

Tubuloînterstitial Nephritis during the Heterologous Phase of Nephrotoxic Serum Nephritis

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