Special Issue "Cellular Immune Responses in Diseases"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 15 January 2024 | Viewed by 991

Special Issue Editor

Dr. Mafalda Fonseca
E-Mail Website
Guest Editor
Health Sciences Research Centre, University of Beira Interior (CICS-UBI), 6200-506 Covilhã, Portugal
Interests: immunology; cellular immune responses; chronic diseases

Special Issue Information

Dear Colleagues,

Cellular immune responses are a crucial aspect of the immune system's defence mechanism, maintaining the right balance between protection and auto-control to avoid damaging healthy tissues or inducing chronic inflammation.

In general, these responses involve innate and adaptive mechanisms, like phagocytosis and cell-mediated cytotoxicity, engaging different leukocyte subpopulations, both antigen-specific and antigen-nonspecific cells. Antigen-specific cellular responses are orchestrated by T cells, crucial for the capacity of the organism to distinguish self from nonself. A good example is the rejection of a graft by lymphoid cells as well as graft-versus-host disease. One T cell has subpopulations of cytotoxic effector cells, which can lyse virus-infected or malignant cells. The subpopulations of helper T cells (e.g., Th1, Th2, Th17) have different patterns of effector cytokine-dependent functions after antigen recognition.

An imbalance in the cellular immune system can lead to various conditions, including autoimmune diseases, immunodeficiencies, and chronic inflammatory disorders. We expect that this Special Issue will provide fresh perspectives in the integration of knowledge concerning cellular immune responses and their regulation in disease contexts.

We invite our colleagues to submit original as well as review articles related to both non-communicable diseases/chronic diseases (e.g., neurological diseases, cardiovascular diseases, chronic respiratory diseases, chronic kidney diseases, cancer, diabetes, obesity) and communicable diseases.

Dr. Mafalda Fonseca
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • leukocyte
  • T cells
  • lymphoid cells

Published Papers (1 paper)

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14 pages, 4605 KiB  
Immunological Phenotyping of Mice with a Point Mutation in Cdk4
Biomedicines 2023, 11(10), 2847; https://doi.org/10.3390/biomedicines11102847 - 20 Oct 2023
Viewed by 558
Cyclin-dependent kinases (CDKs) play a crucial role in regulation of the mammalian cell cycle. CDK4 and CDK6 control the G1/S restriction checkpoint through their ability to associate with cyclin D proteins in response to growth factor signals. CDK4 deficiency in mice gives rise [...] Read more.
Cyclin-dependent kinases (CDKs) play a crucial role in regulation of the mammalian cell cycle. CDK4 and CDK6 control the G1/S restriction checkpoint through their ability to associate with cyclin D proteins in response to growth factor signals. CDK4 deficiency in mice gives rise to a range of endocrine-specific phenotypes including diabetes, infertility, dwarfism, and atrophy of the anterior pituitary. Although CDK6 deficiency can cause thymic atrophy due to a block in the double-negative (DN) to double-positive (DP) stage of T cell development, there are no overt defects in immune cell development reported for CDK4-deficient mice. Here, we examined the impact of a novel N-ethyl-N-nitrosourea-induced point mutation in the gene encoding CDK4 on immune cell development. Mutant mice (Cdk4wnch/wnch) showed normal development and differentiation of major immune cell subsets in the thymus and spleen. Moreover, T cells from Cdk4wnch/wnch mice exhibited normal cytokine production in response to in vitro stimulation. However, analysis of the mixed bone marrow chimeras revealed that Cdk4wnch/wnch-derived T cell subsets and NK cells are at a competitive disadvantage compared to Cdk4+/+-derived cells in the thymus and periphery of recipients. These results suggest a possible role for the CDK4wnch mutation in the development of some immune cells, which only becomes apparent when the Cdk4wnch/wnch mutant cells are in direct competition with wild-type immune cells in the mixed bone marrow chimera. Full article
(This article belongs to the Special Issue Cellular Immune Responses in Diseases)
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