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Drawing on recent research on determinants of subjective well-being, we developed and conducted a pilot study of an employee well-being questionnaire using M. Seligman's (2011) Positive psychology is a quite new branch of psychology the roots of which can be traced back to Martin E. P. Seligman's 1998 Presidential Address to the American Psychological Association (Seligman, 1998). As APA president, Seligman initiated a shift in psychology's focus toward more positive psychological topics, such as well-being, contentment, hope, optimism, flow, happiness, savouring, human strengths, and resilience. In contrast with the classical focus of psychology on curing mental illness, positive psychology emphasizes understanding the factors that build strengths, help people to flourish and contribute to mental health, as well as on subjective wellbeing and happiness. All of these factors and processes may underlie optimal human functioning. (Seligman, 2002, p. 4). The message of the positive psychology movement is to remind our field that it has been deformed. Psychology is not just the study of disease, weakness, and damage; it also is the study of strength and virtue. Treatment is not just fixing what is wrong; it also is building what is right. Psychology is not just about illness or health; it also is about work, education, insight, love, growth, and play. And in this quest for what is best, positive psychology does not rely on wishful thinking, selfdeception, or hand waving; instead, it tries to adapt what is best in the scientific method to the unique problems that human behavior presents in all its complexityConsidering the basic statement Seligman proposed, how can we define positive psychology? There are as many definitions as there are positive psychologists, for example: "Positive psychology is a scientific field that studies the optimal functioning of individuals, groups, and institutions" (Gable and Haidt, 2005).

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Aging is associated with reduced trapping of Ag in the form of in immune complexes (ICs) by follicular dendritic cells (FDCs). We postulated that this defect was due to altered regulation of IC trapping receptors. The level of FDC-M1, complement receptors 1 and 2, FcγRII, and FDC-M2 on FDCs was immunohistochemically quantitated in draining lymph nodes of actively immunized mice for 10 days after Ag challenge. Initially, FDC FcγRII levels were similar but by day 3 a drastic reduction in FDC-FcγRII expression was apparent in old mice. FDC-M2 labeling, reflecting IC trapping, was also reduced and correlated with a dramatic reduction in germinal center (GC) B cells as indicated by reduced GC size and number. Nevertheless, labeling of FDC reticula with FDC-M1 and anti-complement receptors 1 and 2 was preserved, indicating that FDCs were present. FDCs in active GCs normally express high levels of FcRs that are thought to bind Fc portions of Abs in ICs and minimize their binding to FcRs on B cells. Thus, cross-linking of B cell receptor and FcR via IC is minimized, thereby reducing signaling via the immunoreceptor tyrosine-based inhibition motif. Old FDCs taken at day 3, when they lack FcγRII, were incapable of preventing immunoreceptor tyrosine-based inhibition motif signaling in wild-type B cells but old FDCs stimulated B cells from FcγRIIB−/− mice to produce near normal levels of specific Ab. The present data support the concept that FcR are regulated abnormally on old FDCs. This abnormality correlates with a reduced IC retention and with a reduced capacity of FDCs to present ICs in a way that will activate GC B cells.