Leukocytes of the innate immune system play a central protective role in immune defense to pathogens but may also mediate injurious inflammatory responses resulting in tissue injury. These leukocytes provide the first rapid cellular defense mechanisms through a limited repertoire of rapid pre-programmed responses, but they are also involved in chronic inflammation and tissue repair. They are directed to sites of pathogen challenge and inflammation by a variety of mechanisms and are activated in response to both exogenous and endogenous stimuli. They do not show the capacity of self-non-self discrimination and memory, which are defining characteristics of the adaptive immune system, although macrophages in particular may show some capacity for differentiation of their effector responses. However, they do play an integral role in adaptive immune responses by their capacity to present antigen, modify T-cell development, and function as effectors of adaptive cell-mediated immunity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s00281-007-0097-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Novel carbon dots with dual Modulatory effects on the bone marrow and spleen as a potential therapeutic candidate for treating spinal cord injury.
Bioact Mater
March 2025
Tianjin Key Laboratory of Spine and Spinal Cord, International Science and Technology Cooperation Base of Spinal Cord Injury, Department of Orthopedics, International Chinese Musculoskeletal Research Society Collaborating Center for Spinal Cord Injury, Tianjin Medical University General Hospital, Tianjin, 300070, China.
Spinal cord injury triggers leukocyte mobilization from the peripheral circulation to the injury site, exacerbating spinal cord damage. Simultaneously, bone marrow hematopoietic stem cells (HSCs) and splenic leukocytes rapidly mobilize to replenish the depleted peripheral blood leukocyte pool. However, current treatments for spinal cord injuries overlook interventions targeting peripheral immune organs and tissues, highlighting the need to develop novel drugs capable of effectively regulating peripheral immunity and treating spinal cord injuries.
View Article and Find Full Text PDFComplement activation drives the phagocytosis of necrotic cell debris and resolution of liver injury.
Front Immunol
December 2024
Laboratory of Molecular Immunology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium.
Cells die by necrosis due to excessive chemical or thermal stress, leading to plasma membrane rupture, release of intracellular components and severe inflammation. The clearance of necrotic cell debris is crucial for tissue recovery and injury resolution, however, the underlying mechanisms are still poorly understood, especially . This study examined the role of complement proteins in promoting clearance of necrotic cell debris by leukocytes and their influence on liver regeneration.
View Article and Find Full Text PDFEscape of Kdm6a from X Chromosome Is Detrimental to Ischemic Brains via IRF5 Signaling.
Transl Stroke Res
January 2025
Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
The role of chromatin biology and epigenetics in disease progression is gaining increasing recognition. Genes that escape X chromosome inactivation (XCI) can impact neuroinflammation through epigenetic mechanisms. Our previous study has suggested that the X escapee genes Kdm6a and Kdm5c are involved in microglial activation after stroke in aged mice.
View Article and Find Full Text PDFCirculating biomarkers associated with pediatric sickle cell disease.
Front Mol Biosci
December 2024
Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, United States.
Introduction: Sickle cell disease (SCD) is a genetic blood disorder caused by a mutation in the HBB gene, which encodes the beta-globin subunit of hemoglobin. This mutation leads to the production of abnormal hemoglobin S (HbS), causing red blood cells to deform into a sickle shape. These deformed cells can block blood flow, leading to complications like chronic hemolysis, anemia, severe pain episodes, and organ damage.
View Article and Find Full Text PDFChitooligosaccharides promote diabetic wound healing by mediating fibroblast proliferation and migration.
Sci Rep
January 2025
Department of Burn and Plastic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, People's Republic of China.
Diabetic wounds are notoriously difficult to heal due to impaired cell repair mechanisms, reduced angiogenesis, and a heightened risk of infection. Fibroblasts play a vital role in wound healing by producing extracellular matrix (ECM) components and various growth factors, but their function is inhibited in diabetic wounds. Chitooligosaccharides (COS), intermediate products of chitosan degradation, have shown efficacy in promoting tissue repair, yet their role in diabetic wound healing remains underexplored.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!