CD4 T Cells Induce A Subset of MHCII-Expressing Microglia that Attenuates Alzheimer Pathology
Open accessAbstract
Microglia play a key role in innate immunity in Alzheimer disease (AD), but their role as antigen-presenting cells is as yet unclear. Here we found that amyloid β peptide (Aβ)-specific T helper 1 (Aβ-Th1 cells) T cells polarized to secrete interferon-γ and intracerebroventricularly (ICV) injected to the 5XFAD mouse model of AD induced the differentiation of major histocompatibility complex class II (MHCII)+ microglia with distinct morphology and enhanced plaque clearance capacity than MHCII- microglia. Notably, 5XFAD mice lacking MHCII exhibited an enhanced amyloid pathology in the brain along with exacerbated innate inflammation and reduced phagocytic capacity. Using a bone marrow chimera mouse model, we showed that infiltrating macrophages did not differentiate to MHCII+ cells following ICV injection of Aβ-Th1 cells and did not support T cell-mediated amyloid clearance. Overall, we demonstrate that CD4 T cells induce a P2ry12+ MHCII+ subset of microglia, which play a key role in T cell-mediated effector functions that abrogate AD-like pathology.
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MHCII+ microglia have higher phagocytosis rates than MHCII− microglia in 5xFAD mice.
“MHCII+ microglia exhibited higher rates of phagocytosis than their MHCII− counterparts in 5xFAD mice (60).”
From Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model (2025) · cites this paper as [60]
The Results (Figure 2B; page not available in our copy) report greater Aβ co-localization and engulfment by MHCII+ than MHCII− cells, which the authors interpret as presumably indicating greater phagocytic activity. The comparison was made in 5XFAD mice injected with Aβ-specific Th1 cells, and the paper measured co-localization rather than phagocytosis rates directly; the citing sentence omits those qualifications. (LLM, conf=0.88)
Experimental — accuracy not yet measuredDepletion of T cells, B cells, and natural killer (NK) cells contributes to an increase in Aβ deposition.
“It has previously been shown that the depletion of T cells, B cells, and natural killer (NK) cells contributes to an increase in Aβ deposition [4–6].”
From Control of the temporal development of Alzheimer’s disease pathology by the MR1/MAIT cell axis (2023) · cites this paper as [6]
The Results section ('MHCII-Knockout 5XFAD Mice Exhibit an Exacerbated Amyloid Pathology'; page unavailable) reports increased Aβ plaques in mice lacking MHCII. The Discussion reports reduced Aβ uptake in a mouse model lacking adaptive immunity. Neither passage shows that depletion of T cells, B cells, and NK cells together increased Aβ deposition; in particular, the cited paper does not report NK-cell depletion. (LLM, conf=0.85)
Experimental — accuracy not yet measured5XFAD mice that lack MHC class II expression exhibit increased amyloid pathology.
“a recent study found that 5XFAD mice that lack MHC class II expression exhibit increased amyloid pathology, 21”
From The P522R protective variant of PLCG2 promotes the expression of antigen presentation genes by human microglia in an Alzheimer's disease mouse model (2022) · cites this paper as [21]
Loss of MHC class II molecules increases Aβ plaques.
“Notably, the loss of MHC class II molecules has been shown to increase Aβ plaques [3, 6].”
From Control of the temporal development of Alzheimer’s disease pathology by the MR1/MAIT cell axis (2023) · cites this paper as [6]
Adoptive transfer of T helper 1 (Th1) cells into AD model mice results in a decrease in the amount of Aβ.
“Adoptive transfer of T helper 1 (Th1) cells into AD model mice results in a decrease in the amount of Aβ [6].”
From Control of the temporal development of Alzheimer’s disease pathology by the MR1/MAIT cell axis (2023) · cites this paper as [6]
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Lee, E. J., Bae, S., Suh, M., Choi, H., Choi, Y., Hwang, D. W., & Lee, D. S. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.01.20.524845 · Cited by 1 · see citing works
- Authors
- Mittal, K., Eremenko, E., Berner, O., Elyahu, Y., Strominger, I., Apelblat, D., Nemirovsky, A., Spiegel, I., & Monsonego, A.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- Weizmann Institute of Science (IL)
- Corresponding author
- Monsonego, Alon
- ORCID
- Venue
- iScience
- Publisher
- Elsevier BV
- Published
- 2019-06
- Volume
- 16
- Pages
- 298-311
- ISSN
- 2589-0042 (ISSN-L)
- PMC
- PMC6581663
- OpenAlex
- W2947933080
- Cited by
- 114
- References
- 76
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 28 · 2023: 17 · 2022: 16 · 2021: 10 · 2020: 13
- FWCI
- 4.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- iScience (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Israel Science Foundation (684/14)
- Litwin and Gural Foundations
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- Alzheimer's disease, microglia, CD4+ T cells, MHC class II, amyloid-beta, Th1 cells, interferon-gamma, amyloid plaque clearance, P2Y12 receptor, 5xFAD mice, innate immunity, phagocytosis, bone marrow chimeras, infiltrating macrophages
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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