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The Molecular Roles of CD4+ T Cell Subsets in Neuropathological Diseases—Unraveling Diverse Interactions and Therapeutic Potentials

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Dear Colleagues,

We are pleased to announce a call for papers for a Special Issue in the MDPI Journal CIMB on the topic “The Molecular Roles of CD4+ T Cell Subsets in Neurodegenerative Diseases”. This Special Issue aims to comprehensively explore the multifaceted roles of CD4+ T cell subsets, including Th17, Th1, Th2, Th9, and Th22, in the pathogenesis of various neurodegenerative disorders.

Neurodegenerative diseases, such as multiple sclerosis, Parkinson’s, Alzheimer’s, and depression, involve complex immune responses that impact neuronal integrity and function. Th17 and Th1 cells have emerged as key pro-inflammatory mediators, driving chronic neuroinflammation and contributing to neuronal damage and astrogliosis in several neurodegenerative conditions. Conversely, Th2 cells may exert regulatory effects, modulating the inflammatory response and potentially providing neuroprotection. The roles of Th9 and Th22 cells in these diseases remain less explored, and a deeper understanding of their contributions to neuroinflammation could unveil novel therapeutic targets. Additionally, regulatory T cells (Treg) hold significant promise as they exhibit potent anti-inflammatory properties, suppress excessive immune responses, and maintain immune tolerance.

In this Special Issue, we invite original research articles, reviews, and perspective pieces that delve into the molecular mechanisms underlying the interactions of CD4+ T cell subsets with neural components, including neurons, glia, astrocytes, pericytes oligodendrocytes, and the blood–brain barrier (BBB). Topics of interest include but are not limited to:

Signaling pathways and immune responses initiated by CD4+ T cell subsets in neurodegenerative diseases;
Crosstalk between CD4+ T cells and neural cells influencing neuroinflammation and neuronal and/or glial damage;
Implications of CD4+ T cell dysregulation on BBB integrity and permeability;
Therapeutic potentials of targeting CD4+ T cell subsets, including Treg, to mitigate neuroinflammation and preserve neural function.

Dr. Michel-Edwar Mickael
Guest Editor

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16 pages, 887 KiB

Open AccessHypothesis

The Current Landscape of Hypotheses Describing the Contribution of CD4+ Heterogeneous Populations to ALS

by Mariusz Sacharczuk, Michel-Edwar Mickael, Norwin Kubick, Agnieszka Kamińska, Jarosław Olav Horbańczuk, Atanas G. Atanasov, Piotr Religa and Michał Ławiński

Curr. Issues Mol. Biol. 2024, 46(8), 7846-7861; https://doi.org/10.3390/cimb46080465 - 23 Jul 2024

Cited by 2 | Viewed by 1275

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a poorly understood and fatal disease. It has a low prevalence and a 2–4 year survival period. Various theories and hypotheses relating to its development process have been proposed, albeit with no breakthrough in its treatment. Recently, the role of the adaptive immune system in ALS, particularly CD4+ T cells, has begun to be investigated. CD4+ T cells are a heterogeneous group of immune cells. They include highly pro-inflammatory types such as Th1 and Th17, as well as highly anti-inflammatory cells such as Tregs. However, the landscape of the role of CD4+ T cells in ALS is still not clearly understood. This review covers current hypotheses that elucidate how various CD4+ T cells can contribute to ALS development. These hypotheses include the SWITCH model, which suggests that, in the early stages of the disease, Tregs are highly capable of regulating the immune response. However, in the later stages of the disease, it seems that pro-inflammatory cells such as Th1 and Th17 are capable of overwhelming Treg function. The reason why this occurs is not known. Several research groups have proposed that CD4+ T cells as a whole might experience aging. Others have proposed that gamma delta T cells might directly target Tregs. Additionally, other research groups have argued that less well-known CD4+ T cells, such as Emoes+ CD4+ T cells, may be directly responsible for neuron death by producing granzyme B. We propose that the ALS landscape is highly complicated and that there is more than one feasible hypothesis. However, it is critical to take into consideration the differences in the ability of different populations of CD4+ T cells to infiltrate the blood–brain barrier, taking into account the brain region and the time of infiltration. Shedding more light on these still obscure factors can help to create a personalized therapy capable of regaining the balance of power in the battle between the anti-inflammatory and pro-inflammatory cells in the central nervous system of ALS patients. Full article

(This article belongs to the Special Issue The Molecular Roles of CD4+ T Cell Subsets in Neuropathological Diseases—Unraveling Diverse Interactions and Therapeutic Potentials)

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