The newborn immune system differs quantitatively and functionally from adults. At birth, the immune system is partially immature, resulting in deficiency in cell-mediated cytolysis, immunoglobulin synthesis and cytokine production. The most clearly defined deficit in neonatal phagocytosis defenses is diminished neutrophil storage. T cell function is diminished, including T cell-mediated cytotoxicity and T cell help for B cell differentiation. Selective decreases in cytokine production by T cells may contribute to all of these deficits. One of the fundamental differences between adults and newborns for T cell functions resides in whether or not the patient had prior exposure to antigens. Significant immune responses to antigens can be obtained in the neonatal period. These responses are qualitatively different from those induced in adults with a predominance of TH2 pattern.
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http://dx.doi.org/10.1016/s0929-693x(99)80241-3 | DOI Listing |
Alzheimers Dement
December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Beckman Research Institute of City of Hope, Duarte, CA, USA.
Background: Brain organoid models were generated from healthy control or Alzheimer's disease patient iPSCs to facilitate our understanding of AD pathogenesis.
Method: ApoE3 and ApoE4 iPSCs were developed into brain organoids using our recently developed brain organoid platform that allows prolonged culture of brain organoids. Human iPSCs were also differentiated into microglia, which were then co-cultured with brain organoids.
Alzheimers Dement
December 2024
The TT & WF Chao Center for BRAIN and Houston Methodist Neal Cancer Center, Houston Methodist Hospital, Houston, TX, USA.
Background: Global epidemiological studies involving over nine million participants have shown a 35% lower incidence of Alzheimer's Disease (AD) in older cancer survivors compared to those without a history of cancer. This inverse relationship, consistent across recent studies with methodological controls, suggests that cancer itself, rather than cancer treatments, may offer protective factors against AD. This insight opens avenues for novel therapeutic strategies targeting early AD by harnessing cancer-associated protective factors.
View Article and Find Full Text PDFBackground: Accumulating evidence suggests that the presynaptic protein α-synuclein (α-syn), is involved in the pathophysiology of AD and elevated in the cerebrospinal fluid (CSF). The role of Natural Killer (NK) cells of the innate immune system in AD has largely been overlooked. In a murine model, depletion of NK cells augmented the accumulation of pathological α-syn.
View Article and Find Full Text PDFHistol Histopathol
December 2024
Laboratory of Anatomy, Department of Basic Veterinary Sciences, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Sex hormones regulate gut function and mucosal immunity; however, their specific effects on the mucosa-associated lymphoid tissue (MALT) in the rectum of mammals remain unclear. Here, we aimed to investigate the influence of sex on MALT in the rectum of mammals by focusing on the rectal mucosa-associated lymphoid tissues (RMALTs) of C57BL/6NCrSIc mice. Histological analysis revealed that RMALTs were predominantly located in the lamina propria and submucosa of the rectal mucosa, with a significant sex-related difference in the distance from the anorectal junction to the first appearance of the RMALT.
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