Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0014070 (
encephalomyelitis
)
13,017
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Innate immune cells may regulate adaptive immunity by balancing different lineages of T cells and providing negative costimulation. In addition, CD11b(+)Gr-1(+) myeloid-derived suppressor cells have been described in tumor, parasite infection, and severe trauma models. In this study, we observe that splenic CD11b(+) cells markedly increase after experimental autoimmune
encephalomyelitis
(EAE) immunization, and they suppress T cell proliferation in vitro. Although >80% of CD11b(+) cells express varying levels of Gr-1, only a small population of CD11b(+)Ly-6C(high) inflammatory monocytes (IMC) can efficiently suppress T cell proliferation and induce T cell apoptosis through the production of NO. IFN-gamma produced by activated T cells is essential to induce IMC suppressive function. EAE immunization increases the frequencies of IMC in the bone marrow, spleen, and blood, but not in the lymph nodes. At the peak of EAE, IMC represent approximately 30% of inflammatory cells in the CNS. IMC express F4/80 and
CD93
but not CD31, suggesting that they are immature monocytes. Furthermore, IMC have the plasticity to up-regulate NO synthase 2 or arginase 1 expression upon different cytokine treatments. These findings indicate that CD11b(+)Ly-6C(high) IMC induced during EAE priming are powerful suppressors of activated T cells. Further understanding of suppressive monocytes in autoimmune disease models may have important clinical implications for human autoimmune diseases.
...
PMID:CD11b+Ly-6C(hi) suppressive monocytes in experimental autoimmune encephalomyelitis. 1791 8
Microglia and non-professional immune cells (endothelial cells, neurons) participate in the recognition and removal of pathogens and tissue debris in the injured central nervous system through major pro-inflammatory processes. However, the mechanisms involved in regulating these responses remain ill-characterized. We herein show that
CD93
, also known as complement C1qRp/AA4 stem cell marker, has an important role in the regulation of inflammatory processes. The role of
CD93
was evaluated in two models of neuroinflammation. We used the MOG-experimental autoimmune
encephalomyelitis
(EAE) model and the antibody-dependent EAE (ADEAE), which were induced in wild-type and
CD93
knockout mice. We found that
CD93
was highly expressed by neurons, endothelial cells and microglia (ramified >> amoeboid). Astrocytes and oligodendrocytes did not to express
CD93
. We further observed that
CD93
-deficient (
CD93
-/-
) mice presented a more robust brain and spinal cord inflammation in EAE and ADEAE. Encephalitis in
CD93
-/-
was characterized by increased numbers of infiltrating M1 macrophages (CD11c
+
CD206
-
) and amoeboid microglia exhibiting a more activated phenotype (Tomato Lectin
high
Cox2
high
). Damage to and leakage through the blood-brain barrier was increased in
CD93
-/-
animals and was associated with a more robust neuronal injury when compared with wild-type EAE mice. We propose that
CD93
is an important neuro-immune regulator to control central nervous system inflammation.
...
PMID:CD93 regulates central nervous system inflammation in two mouse models of autoimmune encephalomyelitis. 2992 17
