What is the clinical evidence from this study?

Study design: Other. Population: Atherosclerosis. Intervention: MHCII deficiency vs. ApoE −/− mice. Primary outcome: Atherosclerosis as assessed by en face Oil Red O staining of the aorta (p=<0.01).

What question did this study set out to answer?

This study aims to investigate how the lack of major histocompatibility complex class II (MHCII) affects atherosclerosis in mice.

July 25, 2026Circulation

Lack of Ability to Present Antigens on Major Histocompatibility Complex Class II Molecules Aggravates Atherosclerosis in ApoE −/− Mice

Q: What are the key findings of this study?

MHCII deficiency in ApoE −/− mice significantly aggravated atherosclerosis, increasing aortic lesion area from 1.9% to 4.7% (P<0.01), primarily due to the loss of regulatory T cells.

Q: What question did this study set out to answer?

This study aims to investigate how the lack of major histocompatibility complex class II (MHCII) affects atherosclerosis in mice.

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Key result

MHCII deficiency increases aortic atherosclerosis ~150% via regulatory T-cell loss.

P<0.01

Why the study?

Does MHCII deficiency aggravate atherosclerosis in ApoE-/- mice?

Population

Apolipoprotein E (ApoE-/-) mice

Comparison

Deficiency for major histocompatibility complex… vs ApoE-/- mice with intact MHCII

Design

Preclinical

Authors

MWMaria WigrenHebei Medical University SRSara RattikScania (Sweden)IMIngrid Yao MattissonSkåne University Hospital

Discussion

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Implication

Antigen presentation on MHCII has protective functions in atherosclerosis, primarily through activation of regulatory T cells, suggesting potential cardiovascular risks associated with immunosuppressive therapy.

Key Points

This study aims to investigate how the lack of major histocompatibility complex class II (MHCII) affects atherosclerosis in mice.
Apolipoprotein E (ApoE −/−) mice deficient for MHCII were used to assess the role of MHCII in atherosclerosis development.
En face Oil Red O staining was performed to quantify atherosclerosis in the aorta.
Cell transfer and blocking antibody experiments were conducted to understand the impact of regulatory T cells.
ApoE −/− MHCII −/− mice exhibited atherosclerosis levels of 4.7±2.9% compared to 1.9±1.3% in ApoE −/− mice (P <0.01).
The cross-sectional area of subvalvular lesions in ApoE −/− MHCII −/− mice was 7.7±2.2×10 5 µm 2 versus 4.6±2.8×10 5 µm 2 in the control group (P <0.05).
Loss of regulatory T cells was identified as a major factor contributing to increased atherosclerosis severity.

Structured PICO

Does MHCII deficiency aggravate atherosclerosis in ApoE-/- mice?

Population

ApoE −/− mice deficient for MHCII (ApoE −/− MHCII −/−) used to study the role of MHCII in atherosclerosis development.

Exposure

Deficiency for major histocompatibility complex class II (MHCII) (ApoE-/- MHCII-/-)

Comparator

ApoE-/- mice with intact MHCII

Outcome

Atherosclerosis development assessed by en face Oil Red O staining of the aorta and cross-sectional area of subvalvular lesionssurrogate

Main Result

Absolute Event Rate: 4.7% vs 1.9%

p-value: p=<0.01

Cite This Study

Wigren et al. (2019) studied Atherosclerosis. MHCII deficiency vs. ApoE −/− mice was evaluated on Atherosclerosis as assessed by en face Oil Red O staining of the aorta (p=<0.01). MHCII deficiency in ApoE −/− mice significantly aggravated atherosclerosis, increasing aortic lesion area from 1.9% to 4.7% (P<0.01), primarily due to the loss of regulatory T cells.

synapsesocial.com/papers/6a642b2e978f241269770a85 https://doi.org/10.1161/circulationaha.118.039288

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Lack of Ability to Present Antigens on Major Histocompatibility Complex Class II Molecules Aggravates Atherosclerosis in ApoE −/− Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Lack of Ability to Present Antigens on Major Histocompatibility Complex Class II Molecules Aggravates Atherosclerosis in ApoE −/− Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

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