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Defective dendritic cell accessory function in NZB/W F1 hybrid mice
R Phillips1, R Lomnitzer, A R Rabson
1Medical Research Council Human Cellular Immunology Unit, School of Pathology, South African Institute for Medical Research, Johannesburg.
Journal of Clinical & Laboratory Immunology
|March 1, 1988
Summary
NZB/W F1 hybrid mice show defective T cell proliferation when stimulated by sodium periodate (NaIO4). This defect stems from impaired splenic dendritic cells (DC), not T cells themselves, impacting immune responses.
Area of Science:
- Immunology
- Cell Biology
Background:
- NZB/W F1 hybrid mice are a model for autoimmune diseases.
- T cell proliferation is crucial for adaptive immunity.
Purpose of the Study:
- To investigate the cause of defective T cell proliferation in NZB/W F1 mice upon sodium periodate (NaIO4) stimulation.
- To differentiate between intrinsic T cell defects and accessory cell defects.
Main Methods:
- Sodium periodate (NaIO4) was used to activate splenic T cells.
- Dendritic cells (DC) were purified from NZB/W F1 and NZW mice.
- T cell proliferation was assessed using 3H-thymidine incorporation in co-culture experiments.
Main Results:
- NZB/W F1 mice exhibited a markedly defective proliferative response to NaIO4 compared to NZW mice.
- Normal NZW dendritic cells restored the T cell response in NZB/W F1 mice.
- NZB/W F1 dendritic cells failed to support T cell activation in NZW mice.
Conclusions:
- The defect in T cell activation by NaIO4 in NZB/W F1 mice is due to impaired accessory function of splenic dendritic cells.
- Dendritic cell dysfunction contributes to the immunological abnormalities observed in NZB/W F1 mice.