Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Z Rheumatol. 2005 May;64(4):249-54.

[T cell-dependent monocyte activation, TNFalpha and apolipoprotein A-I in autoimmunity and inflammation].

[Article in German]

Author information

  • 1Medizinische Klinik und Poliklinik IV, Zentrum für Innere Medizin der Universität Leipzig, Liebigstr. 22, 04103, Leipzig, Germany.


Rheumatoid arthritis is characterized by a massive overproduction of monokines like TNFalpha, IL-6 and IL-1beta, which are predominantly produced by monocytes and macrophages. To date, the exact mechanisms of monocyte/macrophage activation have not been fully elucidated. One possible mechanism is their cell contact-dependent activation by activated T cells. The direct cell contact of monocytes/macrophages and T cells leads to an increased production of pro-inflammatory cytokines such as TNFalpha and IL-1beta. Stringent control of this mechanism by inhibitory factors appears mandatory under physiological conditions in order to avoid systemic cytokine release syndromes. The presence of inhibitory factors in the serum could represent such a mechanism. In healthy donors, apolipoprotein A-I was identified as such an inhibitory serum protein. In patients with rheumatoid arthritis, apolipoprotein A-I is found in decreased concentrations, possibly due to its role as a negative acute phase protein. The role of this and other inhibitory serum molecules are discussed.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Icon for Springer
    Loading ...
    Write to the Help Desk