Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism (2nd Edition)
A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".
Deadline for manuscript submissions: 15 February 2026 | Viewed by 591
Special Issue Editor
Interests: mycobacterial diseases; tuberculosis; host immune responses; pathogenesis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Immunologists have long been puzzled by the self-destructive nature of the inflammatory response. Inflammation can be elicited by various harmful stimuli, such as microbial/viral infections, allergic reactions, chemical insults, lipotoxicity, tissue damage, or other traumas. Breaking down damaged cells and converting them into various nutrients for tissue regeneration is one of the most important functions of the human immune system to maintain health. A localized inflammatory response is protective if the human immune system can effectively eliminate harmful stimuli and initiate healing. Cell self-destruction (programmed cell death) includes apoptosis, pyroptosis, necroptosis, necrosis, etc. Phagocytosis removes various cell debris produced by cell self-destruction and converts these debris into nutrients. The immune system thus becomes a powerful nutrient generator. At this time, digestion and immunity are interrelated and integrated and play the essential role of disease prevention and immunonutrition acquisition. In the event of microbial/viral infections, the nutritional flux produced by infected host cell self-destruction (inflammation) may be much greater than those produced by normal apoptosis and much greater than the nutrition provided by daily food intake. Thus, infection-induced inflammation may induce illness-associated anorexia to avoid overnutrition. When the nutrition generated by the degradation of infection-damaged cells exceeds the nutritional requirements of tissue regeneration, most of the excess nutrients will be converted into lipid intermediates. Lipid intermediates will invade healthy non-adipose tissue, leading to lipotoxicity and further tissue damage. In such a case, the inflammatory response's main product (lipid intermediates) is also a strong harming stimuli for tissue/cell damage, amplified during the inflammatory response, forming a vicious cycle, making the inflammatory response extremely destructive. The state of overnutrition will be exacerbated by the loss of lean body mass, coupled with excess lipid intermediates spillover into healthy tissues and organs, exacerbating the inflammatory response, which is characteristic of critically ill or injured patients and in most autoimmune diseases.
In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: microbial/viral infection-induced host cell self-destruction as immunonutrition; programmed cell death and nutrient generation; and cell self-destruction in illness, transient over-nutrition, lipotoxicity, and involuntary weight loss.
Prof. Dr. Vishwanath Venketaraman
Guest Editor
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Keywords
- autoimmunity
- cell self-destruction
- infection
- inflammation
- immunonutrition
- lipotoxicity
- metabolism
- programmed cell death
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