AI Article Synopsis
- SLAM is a protein on hemopoietic cells that regulates immune responses through its interaction with SLAM-associated protein (SAP), affecting how the immune system reacts to stimuli.
- It is usually present on these cells but is quickly boosted during infections or inflammation, playing a key role in the formation of the immunological synapse.
- Deficiencies in the SLAM-SAP pathway are linked to autoimmune diseases and other immune response issues, and while it was believed to promote Th1 responses, this review argues it actually favors Th2 responses while suppressing Th1 activity.
Article Abstract
The signaling lymphocytic activation molecule (SLAM), present on the surface of hematopoietic cells, can regulate some events of the immune responses. This modulatory action is associated with the capacity of SLAM to interact with an intracytoplasmic adapter, such as SLAM-associated protein (SAP). SLAM is constitutively expressed in most of these cells, is rapidly induced after antigenic or inflammatory stimuli, and participates in the immunological synapse. Defects in the function of the SLAM-SAP pathway contribute to immunological abnormalities, resulting in autoimmune diseases, tumors of the lymphoid tissues and inadequate responses to infectious agents. Initially, the role of SLAM was investigated using an anti-SLAM monoclonal antibody (α-SLAM mAb) identified as an agonist of the SLAM-SAP pathway, which could induce the production of interferon-γ and could redirect the immune response to a T helper 1 (Th1) cell profile. However, in this review we postulate that the SLAM-SAP pathway primarily induces a Th2 response and secondarily suppresses the Th1 response.
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