The major rheumatoid factor cross-reactive idiotype is dominantly expressed by Staphylococcus aureus Cowan strain I-activated CD5+ control B cells

Bonagura, Vincent R.; Pernis, Benvenuto; Agostino, Nicodemo; Hatam, Lynda

doi:10.1016/0008-8749(92)90204-3

Cited by 2 publications

(1 citation statement)

References 20 publications

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“…Cross-reactive autoantibody production by B-la cells is well established. Stimulation of normal peripheral blood B cell in vitro with Staphylococcus Aureus, Cowens strain produces a high percentage of WA Xld + B-1 a cells [20]. A high incidence of lymphoid nodules with typical lymphoid follicle architecture have been found in chronic active hepatitis C [21] and more recently in liver biopsies from patients with HCV positive Type II cryoglobulinemia [22].…”

Section: Hypothesis On the Role Of Hepatitis C Virus In The Aetiologymentioning

confidence: 99%

The Aetiology of Mixed Cryoglobulinaemia Associated with Hepatitis C Virus Infection

Agnello

1995

Scand J Immunol

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A strong association of hepatitis C infection (HCV) with 'essential' mixed cryoglobulinaemia has been established. The demonstration of HCV in Type II mixed cryoglobulins with monoclonal rheumatoid factors (mRF) that bear the WA crossidiotype has lead to the hypothesis that mixed cryoglobulins result from chronic stimulation by HCV-lipoprotein of a population of XId WA+B-1a cells. The reactivity of WA IgM initially produced is with the HCV-self antigen complex with RF activity resulting secondarily from the pausi-mutational process accompanying the T cell independent process. This benign proliferation progresses by multi step mutations to malignancy in a minority of patients. The implications of the hypothesis for understanding the physiology of certain natural auto antibodies and for therapeutic intervention in this disease are discussed.

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Section: Hypothesis On the Role Of Hepatitis C Virus In The Aetiologymentioning

confidence: 99%

The Aetiology of Mixed Cryoglobulinaemia Associated with Hepatitis C Virus Infection

Agnello

1995

Scand J Immunol

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The etiology and pathophysiology of mixed cryoglobulinemia secondary to hepatitis C virus infection

Agnello

1997

Springer Semin Immunopathol

120

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The strong association of HCV infection with MC-II and the selective concentration of the virus with the WA mRF in the cryoglobulins are compelling suggestions that the virus is directly involved in production of the mRF and the pathophysiology of MC-II. There is, however, only limited data on HCV involvement in both processes. In cutaneous vasculitis, which is the most prevalent clinical feature of the disease, there is evidence that complexes of HCV, mRF and IgG are formed in situ from components of the cryoglobulins that are present in the blood in a dissociated state. It is postulated that local factors, cooling and stasis predispose to formation of these lesions in the lower limbs. However, since cutaneous vasculitis does not correlate with cryoglobulin levels and may not be induced by cold challenge, other factors may be involved. In particular, the conditions which activate the vascular endothelial cells, leading to the leukocytoclastic vasculitis, require delineation. In contrast to cutaneous vasculitis, HCV RNA has not been prominently detected in immune complexes in MPGN lesions and has not been detected at all in the peripheral neuropathy lesions. These preliminary observations suggest that different pathophysiological processes are involved in for these lesions than in cutaneous vasculitis. From the correlation of remission of disease with decreased cryoglobulinemia and viremia in treated patients with MC-II, and from immunohistological data on the hepatitic lymphoid follicles in MC-II (see chapter 7), it appears that an antigen-driven benign proliferation of B cells is responsible for production off mRF and cryoglobulinemia. New findings have suggested that one mechanism for developing mixed cryoglobulinemia may be that HCV-VLDL complexes that contain apo E2 are poorly endocytosed by the LDLR, which may be a major route of entry of the virus to the cell; persistence of the complexes in the circulation may then stimulate mRF production. This new hypothesis is based only on initial in vitro observations and require independent confirmation and validation in vivo. From indirect clinical evidence it has also been postulated that mRF in some patients may limit the cytopathology in MC-II, resulting in a lower prevalence of cirrhosis in these patients. These findings suggested another hypothesis, which is that the mRF prevents spread of infection to hepatocytes and other permissive and nonpermissive cells by blocking endocytosis of HCV-VLDL complexes by the LDLR. Furthermore, data on the composition of cryoglobulins, the molecular composition of WA mRF and the characterization of monoclonal B cells in the liver of patients with MC-II (see chapter 7) suggest that a specific population of B cells may be involved in the host response to HCV infection. These are B cells that proliferate with little or no somatic mutations of the immunoglobulin genes, are self-replicating, are stimulated by self antigens in a T cell-independent manner and bear the CD5 marker. The proliferation of this B cell population may be th...

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The major rheumatoid factor cross-reactive idiotype is dominantly expressed by Staphylococcus aureus Cowan strain I-activated CD5+ control B cells

Cited by 2 publications

References 20 publications

The Aetiology of Mixed Cryoglobulinaemia Associated with Hepatitis C Virus Infection

The Aetiology of Mixed Cryoglobulinaemia Associated with Hepatitis C Virus Infection

The etiology and pathophysiology of mixed cryoglobulinemia secondary to hepatitis C virus infection

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