An extension of the mathematical model of immunological tolerance including two categories of B and T helper cells, each having a different lifespan, is presented. The simulated recovery from tolerance is compared with experimental data on B and T helper cell tolerance to human gamma globulin (HGG) induced in adult mice. The performed simulation runs suggest the conclusion that in this case it seems impossible to incorporate a high ratio of both, long-lived B cells and/or short-lived T helper cells, if good agreement with the available experimental data should be preserved.
Systemic lupus erythematosus (SLE) is a complex disease characterized by numerous autoantibodies and clinical involvement in multiple organ systems. The immunological events triggering the onset and progression of clinical manifestations are also complex and multi-step, including breach of tolerance in the adaptive immune system, amplification of autoimmunity through innate and adaptive immune system dysregulation, and end-organ damage.
MicroRNAs are short, 19-24 nucleotide long, RNA molecules capable of regulating the longevity and, to a lesser extent, translation of messenger RNA (mRNA) species. The function of the microRNA network, and indeed, even that of individual microRNA species, can have profoundly different roles in even a single cell type as the microRNA/mRNA composition evolves. As the role of microRNA within T cells has come under increasing scrutiny, several distinct checkpoints have been demonstrated to have a particular reliance on microRNA regulation.
B cells are critical players in the orchestration of properly regulated immune responses, normally providing protective immunity without autoimmunity. Balance in the B cell compartment is achieved through the finely regulated participation of multiple B cell populations with different antibody-dependent and independent functions. Both types of functions allow B cells to modulate other components of the innate and adaptive immune system. Autoantibody-independent B cell functions include antigen presentation, T cell activation and polarization, and dendritic cell modulation.
Alloantibody can be a major barrier to successful organ transplantation; however, therapy to control antibody production or to alter its impact on the allograft remains limited. The goal of this review is to examine the regulatory steps that are involved in the generation of alloreactive B cells, with a specific emphasis on how known mechanisms relate to clinical situations in transplant recipients. Thus, we will examine the process of activation of mature, naÔve B cells and how this relates to de novo antibody production.
Since 1960, clinical organ transplantation has evolved from an experimental procedure to highly successful 'routine', but as technical advances have extended eligibility to more victims of end-stage organ disease, the supply of donor organs has lagged behind. Urgency of need, probability of success and ability to pay are often used to limit waiting lists; without these, as many as 124,000 transplants per year could be performed in the USA alone.
There is ample evidence from human and animal studies demonstrating the downward modulation of immune function concomitant with a variety of stressors. As a consequence, the possible enhancement of immune function by behavioral strategies has generated considerable interest.
To assess the influence of a hypnotic intervention on cellular immune function during a commonplace stressful event, the authors selected 33 medical and dental students on the basis of hypnotic susceptibility. Initial blood samples were obtained during a lower stress period, and a second sample was drawn 3 days before the first major exam of the term. Half of the participants were randomly assigned to hypnotic-relaxation training in the interval between samples.
Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
PURPOSE: Solar UV radiation-induced immunosuppression is considered to be a risk factor for melanoma and nonmelanoma skin cancers. We previously have shown that topical application of (-)-epigallocatechin-3-gallate (EGCG) prevents UV-induced immunosuppression in mice. We studied whether prevention of UV-induced immunosuppression by EGCG is mediated through interleukin 12 (IL-12)-dependent DNA repair. EXPERIMENTAL DESIGN: IL-12 knockout (KO) mice on C3H/HeN background and DNA repair-deficient cells from xeroderma pigmentosum complementation group A (XPA) patients were used in this study.