Journal of Immunology Research

The Role of HLA-Class Ib Molecules in Immune-Related Diseases, Tumors, and Infections


Publishing date
30 May 2014
Status
Published
Submission deadline
10 Jan 2014

Lead Editor

1Laboratory of Oncology, Istituto Giannina Gaslini, Genoa, Italy

2Neuroradiology Unit, Department of Neurosciences and Rehabilitation, Azienda Ospedaliera-Universitaria, Arcispedale Sant’Anna, Ferrara, Italy

3Department of Experimental and Diagnostic Medicine, Section of Microbiology, University of Ferrara, Ferrara, Italy

4Laboratoire d’Immunologie de la TransplantationCEA-DSV-IMETI-SRHI, Hôpital Saint-Louis, Paris, France


The Role of HLA-Class Ib Molecules in Immune-Related Diseases, Tumors, and Infections

Description

HLA-class Ib family includes HLA-E, -F, -G, and -H molecules that, in contrast with high polymorphic HLA-class Ia molecules (HLA-A, -B, and -C), display a limited polymorphism, with a small number of alleles encoding limited functional proteins. Similar to HLA-class Ia molecules, HLA-class Ib molecules bind peptides generated from cytosolic antigens and present them to CD8+ T lymphocytes, but their main function is the regulation of immune responses, both in physiological and pathological conditions.

HLA-G is the best characterized HLA-Ib molecule. It is expressed on fetal cytotrophoblast cells during pregnancy and abrogates maternal NK cell cytotoxicity against fetal tissues. However, HLA-G is also expressed (or released as soluble molecule) by different human tumors. HLA-G interacts with specific receptors on T and B lymphocytes, NK cells, and antigen presenting cells, inhibiting their function.

HLA-E is virtually expressed by all nucleated cells and binds peptides derived from HLA-class I molecules leader sequence. In physiological conditions, it interacts with CD94/NKG2A inhibitory receptor on NK cells, inhibiting their cytotoxicity against cells displaying normal HLA-class I molecules expression. When such molecules are downregulated (i.e., transformed or infected cells), HLA-class I-derived peptides are lower, and subsequently HLA-E expression is dampened, allowing NK cells to lyse these cells. However, different transformed cells upregulate HLA-E expression to avoid NK cell-mediated lysis.

Limited information is available regarding HLA-F function. This molecule acts as chaperone for the β2-microglobulin-free heavy chain of other HLA-class I molecules, and it is expressed on the surface of activated lymphocytes. So far, no functional HLA-H molecules encoded by HLA-H genes have been characterized.We are interested in articles that explore novel aspects of HLA-Ib molecules function. Potential topics include, but are not limited to:

  • Expression and function of HLA-Ib molecules in pathological conditions that have not yet been investigated, including tumors, infections (virus, bacteria, and other parasites), and autoimmune/inflammatory diseases
  • Interactions between HLA-G, -E, and -F in pathological conditions
  • Novel mechanism of HLA-Ib molecule-mediated immune regulation
  • Possible effects of HLA-Ib molecules on cells that are crucial in pathological settings (i.e., endothelial cells during angiogenesis)
  • Presence of soluble HLA-Ib molecules in biological fluids during disease and their clinical relevance
  • HLA-Ib molecules expression and/or secretion in novel immune-regulatory cell subsets
  • Potential extraimmunological roles of HLA-Ib molecules

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/jir/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/jir/hla/ according to the following timetable:

Journal of Immunology Research
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Acceptance rate11%
Submission to final decision121 days
Acceptance to publication27 days
CiteScore6.000
Journal Citation Indicator0.560
Impact Factor4.1
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