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Cited by 34Neuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research StudiesImmune Response and Inflammation

Are Microglial Cells the Regulators of Lymphocyte Responses in the CNS?

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Almolda, Beatriz, González, Berta, Castellano, Bernardo·2015·Frontiers in Cellular Neuroscience
DOI 10.3389/fncel.2015.00440PMC PMC4644801
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Abstract

The infiltration of immune cells in the central nervous system is a common hallmark in different neuroinflammatory conditions. Accumulating evidence indicates that resident glial cells can establish a cross-talk with infiltrated immune cells, including T-cells, regulating their recruitment, activation and function within the CNS. Although the healthy CNS has been thought to be devoid of professional dendritic cells (DCs), numerous studies have reported the presence of a population of DCs in specific locations such as the meninges, choroid plexuses and the perivascular space. Moreover, the infiltration of DC precursors during neuroinflammatory situations has been proposed, suggesting a putative role of these cells in the regulation of lymphocyte activity within the CNS. On the other hand, under specific circumstances, microglial cells are able to acquire a phenotype of DC expressing a wide range of molecules that equip these cells with all the necessary machinery for communication with T-cells. In this review, we summarize the current knowledge on the expression of molecules involved in the cross-talk with T-cells in both microglial cells and DCs and discuss the potential contribution of each of these cell populations on the control of lymphocyte function within the CNS.

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  • In Alzheimer's disease and aging, microglia and peripheral myeloid cells may express co-stimulatory ligands, but the ligand-receptor architecture within the plaque microenvironment remains incompletely defined.

    “In Alzheimer’s disease and aging, microglia and peripheral myeloid cells may express co-stimulatory ligands, but the ligand–receptor architecture within the plaque microenvironment remains incompletely defined.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [45]

    The section “Expression of Co-stimulatory Molecules in Microglia” (page unavailable) reports microglial CD40 expression in aging and Alzheimer’s disease and identifies gaps in knowledge about other co-stimulatory molecules. It does not establish co-stimulatory ligand expression by peripheral myeloid cells or specifically assess ligand–receptor relationships within the plaque microenvironment. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Microglia may act as local regulators of lymphocyte activation, particularly when blood-brain barrier dysfunction or chronic neuroinflammation allows greater immune-cell trafficking into the CNS.

    “Reviews of microglia–lymphocyte communication have emphasized that microglia may act as local regulators of lymphocyte activation, particularly when blood–brain barrier dysfunction or chronic neuroinflammation allows greater immune-cell trafficking into the CNS.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [45]

    The section “Expression of MHCs in Microglia” says microglia can regulate infiltrating T-cells’ recruitment, activation and function. The Abstract and “Infiltration of Lymphocytes in the CNS Under Pathological Situations” link immune-cell infiltration to neuroinflammatory and other pathological conditions. The passages do not establish the more specific claim that blood–brain barrier dysfunction permits greater trafficking; no page numbers are available in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • At least some plaque-associated microglia may borrow elements of lymphoid signaling logic rather than merely presenting antigen to lymphocytes.

    “The recent finding therefore suggests that at least some plaque-associated microglia may borrow elements of lymphoid signaling logic rather than merely presenting antigen to lymphocytes [44,45,46].”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [45]

    The section on co-stimulatory molecules (page unavailable) reports CD40, an immune co-stimulatory receptor, in activated microglia in Alzheimer’s disease and links microglial CD40 to β-amyloid pathology. This supports a possible connection to immune signaling, but the paper does not identify plaque-associated microglia specifically or establish signaling distinct from their antigen-presenting role. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • CD80 and CD86 are traditionally expressed by antigen-presenting cells and bind CD28 and CTLA-4 on T cells.

    “CD80 and CD86 are traditionally expressed by antigen-presenting cells and bind CD28 and CTLA-4 on T cells.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [45]

  • In inflammatory and neurodegenerative settings, microglia can upregulate antigen-presentation machinery, respond to interferon-γ and other lymphocyte-derived cytokines, and influence T-cell behavior within or near the central nervous system.

    “In inflammatory and neurodegenerative settings, microglia can upregulate antigen-presentation machinery, respond to interferon-γ and other lymphocyte-derived cytokines, and influence T-cell behavior within or near the central nervous system.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [45]

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Authors
Almolda, B., González, B., & Castellano, B.
Affiliations
Universitat Autònoma de Barcelona (ES)
Corresponding author
Almolda, Beatriz
ORCID
Venue
Frontiers in Cellular Neuroscience
Publisher
Frontiers Media SA
Published
2015-11-16
Volume
9
Pages
440-440
ISSN
1662-5102 (ISSN-L)
DOI
10.3389/fncel.2015.00440
PMC
PMC4644801
OpenAlex
W2175819155
Cited by
34
References
181
Citations by year
2025: 5 · 2024: 7 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 3
FWCI
0.27
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Dipòsit Digital de Documents de la UAB (Universitat Autònoma de Barcelona) (submittedVersion, cc-by)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Ministerio de Economía y Competitividad (BFU2011, BFU2014, BFU2014-55459)
  • Ministerio de Ciencia e Innovación (BFU2014-55459, BFU2011-27400)
  • Universitat de Barcelona
  • Universitat Autònoma de Barcelona
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
microglia, dendritic cells, T cell activation, neuroinflammation, lymphocyte recruitment, choroid plexus, perivascular spaces

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