DOI Seite / Zitierlink:
https://doi.org/10.11588/diglit.48120#0040
22 Molecular and Cell Biology of Autoantibodies and Autoimmunity
Immunoregulatory Effects of Borrelia Burgdorferi Antigens in Patients
with Chronic Lyme Disease
J. J. Goronzy, L. Zoller, and C.M. Weyand
Div. of Rheum., Dept of Med., Dept, of Microbiology, University of Heidelberg, FRG
The spirochete Borrelia burgdorferi (BB) has been identified as the causative
infectious agent of Lyme disease. Lyme arthritis is a rheumatic disorder which is
part of a multisystemic disease attributed to a chronic persistent infection with
the spirochete which is tick-transmitted. There is increasing evidence that per-
sisting spirochetal antigen in the synovia is sustaining a chronic destructive im-
mune response. It is unclear whether these patients fail to eliminate the infectious
agent or an autoimmune response is induced by the spirochetal infection. We have
studied T cell responses and requirements for antigen presentation of spirochetal
antigen in patients with Lyme arthritis. Chronic borrelia infection was suspected
in patients with oligoarthritic syndromes who carried IgG antibodies to BB and
had no evidence of spondylarthropathy, psoriatric arthritis or rheumatoid ar-
thritis. Interestingly, only a subgroup of patients carried circulating T lym-
phocytes which proliferated when stimulated with BB-pulsed syngeneic
macrophages. B cells started to proliferate when incubated with ultrasonicated
spirochetal antigen. B cell proliferation was dependend upon HLA-compatible T
cells exluding a LPS-like mitogenic effect of the BB antigen. CD4+ T cells, in-
terleukin 2 and interleukin 4 were able to support the polyclonal B cell response
induced by the spirochetal antigen. The proliferative response was inhibited in the
presence of macrophages and interferon-gamma. These data sugggest that Bor-
relia burgdorferi includes a T-cell dependent B-cell mitogen which might substan-
tially influence the ability of an infected host to process and to present antigen
by activated B cells and might thus initiate an autoimmune reaction.
Molecular Mimicry: A Common Epitope of the (Ul) snRNP Associated
p68 Autoantigen and a Protein of a Human Pathogenic Virus
H.H. Guldner, H.-J. Netter, C. Szostecki, E. Jager, and H. Will
Max-Planck-Institut fiir Biochemie, Am Klopferspitz 18, 8033 Martinsried, FRG
The mechanisms leading to autoimmunity are not known but one possible
concept is crossreaction of antibodies with epitopes shared by microbial antigens
Immunoregulatory Effects of Borrelia Burgdorferi Antigens in Patients
with Chronic Lyme Disease
J. J. Goronzy, L. Zoller, and C.M. Weyand
Div. of Rheum., Dept of Med., Dept, of Microbiology, University of Heidelberg, FRG
The spirochete Borrelia burgdorferi (BB) has been identified as the causative
infectious agent of Lyme disease. Lyme arthritis is a rheumatic disorder which is
part of a multisystemic disease attributed to a chronic persistent infection with
the spirochete which is tick-transmitted. There is increasing evidence that per-
sisting spirochetal antigen in the synovia is sustaining a chronic destructive im-
mune response. It is unclear whether these patients fail to eliminate the infectious
agent or an autoimmune response is induced by the spirochetal infection. We have
studied T cell responses and requirements for antigen presentation of spirochetal
antigen in patients with Lyme arthritis. Chronic borrelia infection was suspected
in patients with oligoarthritic syndromes who carried IgG antibodies to BB and
had no evidence of spondylarthropathy, psoriatric arthritis or rheumatoid ar-
thritis. Interestingly, only a subgroup of patients carried circulating T lym-
phocytes which proliferated when stimulated with BB-pulsed syngeneic
macrophages. B cells started to proliferate when incubated with ultrasonicated
spirochetal antigen. B cell proliferation was dependend upon HLA-compatible T
cells exluding a LPS-like mitogenic effect of the BB antigen. CD4+ T cells, in-
terleukin 2 and interleukin 4 were able to support the polyclonal B cell response
induced by the spirochetal antigen. The proliferative response was inhibited in the
presence of macrophages and interferon-gamma. These data sugggest that Bor-
relia burgdorferi includes a T-cell dependent B-cell mitogen which might substan-
tially influence the ability of an infected host to process and to present antigen
by activated B cells and might thus initiate an autoimmune reaction.
Molecular Mimicry: A Common Epitope of the (Ul) snRNP Associated
p68 Autoantigen and a Protein of a Human Pathogenic Virus
H.H. Guldner, H.-J. Netter, C. Szostecki, E. Jager, and H. Will
Max-Planck-Institut fiir Biochemie, Am Klopferspitz 18, 8033 Martinsried, FRG
The mechanisms leading to autoimmunity are not known but one possible
concept is crossreaction of antibodies with epitopes shared by microbial antigens