当前位置： SCI文献检索 > JOURNAL OF NEUROIMMUNOLOGY期刊下所有文献 > Activated microglial cells acquire an immature dendritic cell phenotype and may terminate the immune response in an acute model of EAE.

Activated microglial cells acquire an immature dendritic cell phenotype and may terminate the immune response in an acute model of EAE.

Abstract：

:Antigen presentation, a key mechanism in immune responses, involves two main signals: the first is provided by the engagement of a major histocompatibility complex (MHC), class I or class II, with their TCR receptor in lymphocytes, whereas the second demands the participation of different co-stimulatory molecules, such as CD28, CTLA-4 and their receptors B7.1 and B7.2. Specific T-cell activation and deactivation are achieved through this signalling. The aim of our study is to characterise, in the acute experimental autoimmune encephalomyelitis (EAE) model in Lewis rat, the temporal expression pattern of these molecules as well as the cells responsible for their expression. To accomplish that, MBP-immunised female Lewis rats were daily examined for the presence of clinical symptoms and sacrificed, according to their clinical score, at different phases during EAE. Spinal cords were cut with a cryostat and processed for immunohistochemistry: MHC-class I and MHC-class II, co-stimulatory molecules (B7.1, B7.2, CD28, CTLA-4) and markers of dendritic cells (CD1 for immature cells and fascin for mature cells). Our results show that microglial cells are activated in the inductive phase and, during this phase and peak, they are able to express MHC-class I, MHC-class II and CD1, but not B7.1 and B7.2. This microglial phenotype may induce the apoptosis or anergy of infiltrated CD28+ lymphocytes observed around blood vessels and in the parenchyma. During the recovery phase, microglial cells express high MHC-class I and class II and, those located in the surroundings of blood vessels, displayed the B7.2 co-stimulatory molecule. These cells are competent to interact with CTLA-4+ cells, which indicate an active role of microglial cells in modulating the ending of the immune response by inducing lymphocyte activity inhibition and Treg activation. Once clinical symptomatology disappeared, some foci of activated microglial cells (MHC-class II+/B7.2+) were still present in concomitance with CTLA-4+ cells, suggesting a prolonged involvement of microglia in lymphocyte inhibition and tolerance promotion. In addition to microglia, during the inductive and recovery phases, we also found perivascular ED2+ cells and fascin+ cells which are able to migrate to the parenchyma and may play a role in lymphocytic regulation. Further studies to understand the specific function played by these cells are warranted.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Almolda B,González B,Castellano B

doi

10.1016/j.jneuroim.2010.03.021

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

39-54

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(10)00133-5

journal_volume

223

pub_type

杂志文章

在线工具

Activated microglial cells acquire an immature dendritic cell phenotype and may terminate the immune response in an acute model of EAE.