Submit a Manuscript to the Journal
For an Article Collection on
Animal Models of Autoimmune Diseases
31 March 2024
Animal Models of Autoimmune Diseases
Autoimmune diseases are syndromes rooted in the loss of immune tolerance to self-antigens that result in pathogenic antibodies and cellular immune responses. They also share a complex etiology that combines genetic and environmental contributions that are not precisely characterized.
Animal models of autoimmune diseases have been developed over the years, most of them in mice. Some inbred strains of mice spontaneously develop an autoimmune pathology similar to the disease presentation in some patients with autoimmune diseases. Genetic engineering has also produced mouse strains in which the deletion or over-expression of specific genes resulted in the development of autoimmune pathology. Finally, induced models have been developed, in many cases to introduce a specific autoantigen in highly inflammatory conditions.
Although the management of autoimmune diseases has improved, their cure still represents a largely unmet medical challenge. The last decade has seen the development of promising therapeutics that offer a significant reduction of disease activity in some patients. Animal models have been used to identify and validate most of these therapeutic targets, as well as to develop and test the efficacy of the therapeutics in pre-clinical settings.
None of the large array of animal models of autoimmune diseases, however, entirely represent the human diseases that they are used for. Selected clinical manifestations presented by patients are presented by specific models, while some are not presented by any models.
This Article Collection addresses the need to reassess the validity and limitations of animal models to study the etiology of autoimmune diseases, to identify and validate therapeutic targets, and to serve as reliable pre-clinical models to test the efficacy of therapeutics. We welcome Research Articles, Review Articles, and Brief Reports. Of particular interest are Review Articles covering any of the topics above.
All manuscripts submitted to this Article Collection will undergo full peer-review; the Guest Advisor will not be handling submitted articles. Please review the journal’s aims and scope and author instructions prior to submission.
Please submit your manuscript through Taylor & Francis's Submission Portal.
During the first step of the submission process (under the "Manuscript Details" heading), you will find the question "Are you submitting your paper for a specific special issue or article collection?" Click the radio button for "Yes".
Next, you will be prompted to select the "Special Issue or Article Collection name" from the dropdown menu. Choose "Animal Models of Autoimmune Diseases" from the list. This will ensure that your manuscript is considered for inclusion.
The manuscript submission deadline is 31 March 2024.
If you have any questions about this Article Collection, please contact Krista Thom at [email protected].
Laurence Morel's research program investigates the mechanisms of lupus pathogenesis using mouse models as well as patient samples, with a focus on CD4 T cells and B cells. The long-term goal of her research is to identify genes or pathways responsible for lupus susceptibility, to characterize their contribution to autoimmune immunopathology, and to translate these findings into therapeutic targets. The most recent work has explored recent work on the genetic, cellular, metabolic and microbial determinants of follicular helper T cell expansion and regulatory T cell impairment in lupus.
Disclosure Statement: Prof. Morel declares no conflict of interest.
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All manuscripts submitted to this Article Collection will undergo desk assessment and peer-review as part of our standard editorial process. Guest Advisors for this collection will not be involved in peer-reviewing manuscripts unless they are an existing member of the Editorial Board. Please review the journal Aims and Scope and author submission instructions prior to submitting a manuscript.