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Comment
. 2001 Jun 18;193(12):F47-50.
doi: 10.1084/jem.193.12.f47.

On the role of the innate immunity in autoimmune disease

M F Bachmann  1 , M Kopf
Affiliations
Comment

On the role of the innate immunity in autoimmune disease

M F Bachmann et al. J Exp Med. .
No abstract available

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Figures

Figure 1
Figure 1
Models for autosensitization of lymphocytes. (a) Self-antigens are transported to lymphoid organs where activation of self-specific lymphocytes occurs. On the left side is indicated that pathogens carrying B or T cell epitopes shared with the host may directly reach lymphoid organs for induction of an immune response. Alternatively, pathogens may infect DCs or are processed by them. Activated DCs subsequently migrate to lymphoid organs and induce autoimmunity. On the right side is illustrated that pathogens may induce cell lysis, either directly or by activation of cytotoxic T cells. Self-antigens (shown in yellow) are released during this process and are taken up and processed by local DCs. In addition, the DCs are stimulated by pathogen-associated patterns triggering their migration to lymphoid organs where autosensitization occurs. (b) Lymphocytes are recruited to the periphery, where activation of self-specific lymphocytes occurs. Chemokines, such as BLC (triangles), are secreted by DCs which attracts B cells from lymphoid organs and probably the peritoneum. B1 cells may be attracted preferentially under these conditions. These B cells together with additionally recruited T cells and the BLC-producing DCs generate an environment ideal for activation of lymphocytes and autosensitization may occur locally.
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