China
Africa
Explore chapters and articles related to this topic
An Introduction to the Immune System and Vaccines
Published in Patricia G. Melloy, Viruses and Society, 2023
In the human body, we have two major branches to the immune system, the innate branch and the adaptive (acquired) branch. The two branches can communicate. Scientists refer to the two aspects of adaptive immune response as humoral immunity (older term referring to bodily fluids) and cell-mediated immunity. Humoral immunity involves two kinds of white blood cells: the B cells that make antibodies and the T cells that are responsible for cell-mediated immunity. Many good reviews or books of the immune system are available (Lostroh 2019; Coico and Sunshine 2015; Nicholson 2016; Marshall et al. 2018; Chaplin 2010).
Autoimmune Disorders across the Lifespan
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
The immune system consists of both the innate and adaptive system. A stronger innate and adaptive immune response in women contributes to an increased susceptibility to AIDs. The innate immune system is the body’s first line of defense and is activated immediately upon exposure of the body to a pathogen. The second line of defense, the adaptive immune system, is acquired, antigen specific, and categorized as humoral or cell mediated. Humoral immunity consists mostly of B cells. Cell-mediated immunity consists of T cells. A subset of T cells known as T helper cells are categorized as Th1 or Th2 and are the major producers of cytokines. Pro-inflammatory cytokines are produced by Th1 cells and anti-inflammatory cytokines are produced by Th2 cells.
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
Immunity provides living organisms with protection from disease.24 Mammals are protected by both innate and adaptive resistance to disease-causing agents. Innate resistance against foreign substances in the skin is provided by mechanical barriers (stratum corneum), secreted products (sweat and sebaceous glands), and inflammatory cells (phagocytes). Adaptive resistance, or acquired immunity, is normally quiescent until stimulated by a specific antigen, and is mediated by specific antibodies or sensitized T lymphocytes. Cell-mediated immunity is one of the two major arms of acquired immunity, and is mediated by sensitized T (thymus-derived) lymphocytes and activated macrophages. The other arm is humoral immunity which is mediated by specific antibodies that are produced by mature B (bursa-equivalent, bone marrow-derived) lymphocytes termed as plasma cells. Resistance to disease requires the involvement of either or both of these arms of the immune system.17 Cell-mediated immunity is protective against viral infected cells, many protozoal and helminth infections, mycobacteria, fungal infections, and certain tumor cells in an immune surveillance (anti-tumor) role.62 Humoral immunity protects against many bacteria and some viruses and protozoa.
MUC1-C integrates type II interferon and chromatin remodeling pathways in immunosuppression of prostate cancer
Published in OncoImmunology, 2022
Masayuki Hagiwara, Atsushi Fushimi, Atrayee Bhattacharya, Nami Yamashita, Yoshihiro Morimoto, Mototsugu Oya, Henry G. Withers, Qiang Hu, Tao Liu, Song Liu, Kwok K. Wong, Mark D. Long, Donald Kufe
In support of MUC1-C involvement in promoting suppression of the PC TME, analysis of the TCGA-PRAD dataset demonstrated that MUC1 associates with enrichment of REACTOME INTERLEUKIN 10 SIGNALING and GO RESPONSE TO TRANSFORMING GROWTH FACTOR BETA pathways (Figure 7a). GSEA confirmed that MUC1-high tumors significantly associate with activation the IL-10 (Supplemental Fig. S8a) and TGFB1 (Supplemental Fig. S8b) gene signatures, which function as negative regulators of the immune TME.9,61 We also found that MUC1-high tumors associate with expression of CCL5 (Supplemental Fig. S8c), an inflammatory chemokine that recruits TAMs, MDSCs and T-regs into the TME and inhibits CTL activity.62 Consistent with these findings, MUC1 was significantly associated with negative regulation of (i) T cell and NK cell mediated immunity, (ii) T cell proliferation, and (iii) B cell activation (Figure 7b). In extending these analyses to the Beltran cohort (67 CRPC/NEPC samples),63 tumors were stratified by MUC1-high and MUC1-low expression. Hierarchical clustering based on cell type estimation (xCell)34 demonstrated that MUC1-high clusters associate with decreased estimates of immune cell infiltration (Figure 7c). Further analysis by immune cell type demonstrated that MUC1-high tumors significantly associate with decreases in CD4+ memory T cells, Th2 cells, B cells and M2 macrophages, among others, as well as the ImmuneScore (Figure 7d; Supplemental Fig. S8d).
Manifestation of Herpetic Eye Disease after COVID-19 Vaccine: A UK Case Series
Published in Ocular Immunology and Inflammation, 2022
Konstantinos I. Rallis, Riccardo Fausto, Darren S. J. Ting, Mouhamed A. Al-Aqaba, Dalia G. Said, Harminder S. Dua
All reported cases of keratitis following vaccination25–27,29 represent stromal (disciform or interstitial) keratitis and are therefore due to a cell-mediated immunological response. Cell-mediated immunity is one of the most important constituents of immunological response to infection and vaccines. Therefore, a key challenge in developing new effective vaccines is to induce optimal memory T-cell responses.37 However, this cell-mediated response is the cause of keratouveitis and uveitis following vaccination against various viruses, including SARS-CoV-2. Recently, we published a case of corneal graft rejection following vaccination against COVID-19 disease, attributed to cell-mediated immunity. In accordance with others,22 we recommended increasing topical steroids following vaccination in patients with recent corneal grafts.23
CD34+ progenitor-derived NK cell and gemcitabine combination therapy increases killing of ovarian cancer cells in NOD/SCID/IL2Rgnull mice
Published in OncoImmunology, 2021
Jolien M.R. Van der Meer, Paul K.J.D. de Jonge, Anniek B. van der Waart, Alexander C. Geerlings, Jurgen P. Moonen, Jolanda Brummelman, Janne de Klein, Malou C. Vermeulen, Ralph J.A. Maas, Nicolaas P.M. Schaap, Janneke S. Hoogstad-van Evert, Petronella B. Ottevanger, Joop H. Jansen, Willemijn Hobo, Harry Dolstra
As ovarian tumors often downregulate MHC class I and express natural killer (NK) cell activating ligands, they are prone to NK cell-mediated immunity.3,4 However, autologous NK cells are often dysfunctional,5 due to tumor-induced immunosuppression and remaining self MHC class I expression on tumor cells. Previously, we demonstrated that umbilical cord blood (UCB)-derived CD34+ hematopoietic progenitor cell (HPC)-NK cells are capable of killing OC monolayers and spheroids.6 Furthermore, we showed that intraperitoneal infusion of HPC-NK cells in human OC-bearing mice significantly limits tumor progression and prolongs survival.6 Currently, we are investigating the feasibility, safety, and toxicity of an intraperitoneal HPC-NK cell infusion in recurrent ovarian cancer patients (NCT:03539406). However, improvement of HPC-NK cell therapy is warranted to maximize the killing of OC cells.