Exploring Play and Playfulness in the Everyday Lives of Older Women

There is an emerging body of literature about older women and play, often focused on social groupings (e.g., Red Hats Society, Raging Grannies). This study aimed to contribute to this body of literature by exploring the meaning, experience, and place of play and playfulness in the day-to-day lives of older women. Interpreting older women’s play as a phenomenologist informed by the feminist gerontology literature, I explored, described, and interpreted play using the voices, words, lived experiences, and artful reflections of four focus groups comprised of nineteen women between the ages of 63 to 95 years. Play emerged to be a wonderful, complex, and paradoxical phenomenon for older women that interconnected in three ways: as a doing, a feeling, and a being. Within and across the women, play was characterized by these paradoxes: time flies by and time slows down, productive and unproductive, social and solitary, and serious and silly. Play was infused into the everyday lives of these older women. Arts-based methods served to invigorate and engage the women and me, and transformed the research environment into a comfortable, open space to play and be playful, and to share, gather, and build knowledge. Thus this research contributes to the growing body of literature about the lives and experiences of older women, from their perspective, adds insight into older women’s play, and grows our knowledge about collecting data through arts-based methods with older women

Atypical and classical memory B cells produce Plasmodium falciparum neutralizing antibodies

Antibodies can protect from Plasmodium falciparum (Pf) infection and clinical malaria disease. However, in the absence of constant reexposure, serum immunoglobulin (Ig) levels rapidly decline and full protection from clinical symptoms is lost, suggesting that B cell memory is functionally impaired. We show at the single cell level that natural Pf infection induces the development of classical memory B cells (CM) and atypical memory B cells (AtM) that produce broadly neutralizing antibodies against blood stage Pf parasites. CM and AtM contribute to anti-Pf serum IgG production, but only AtM show signs of active antibody secretion. AtM and CM were also different in their IgG gene repertoire, suggesting that they develop from different precursors. The findings provide direct evidence that natural Pf infection leads to the development of protective memory B cell antibody responses and suggest that constant immune activation rather than impaired memory function leads to the accumulation of AtM in malaria. Understanding the memory B cell response to natural Pf infection may be key to the development of a malaria vaccine that induces long-lived protection

Plasmodium-specific atypical memory B cells are short-lived activated B cells

A subset of atypical memory B cells accumulates in malaria and several infections, autoimmune disorders and aging in both humans and mice. It has been suggested these cells are exhausted long-lived memory B cells, and their accumulation may contribute to poor acquisition of long-lasting immunity to certain chronic infections, such as malaria and HIV. Here, we generated an immunoglobulin heavy chain knock-in mouse with a BCR that recognizes MSP1 of the rodent malaria parasite, Plasmodium chabaudi. In combination with a mosquito-initiated P. chabaudi infection, we show that Plasmodium-specific atypical memory B cells are short-lived and disappear upon natural resolution of chronic infection. These cells show features of activation, proliferation, DNA replication, and plasmablasts. Our data demonstrate that Plasmodium-specific atypical memory B cells are not a subset of long-lived memory B cells, but rather short-lived activated cells, and part of a physiologic ongoing B-cell response

Atypical and classical memory B cells produce Plasmodium falciparum neutralizing antibodies

Antibodies can protect from Plasmodium falciparum (Pf) infection and clinical malaria disease. However, in the absence of constant reexposure, serum immunoglobulin (Ig) levels rapidly decline and full protection from clinical symptoms is lost, suggesting that B cell memory is functionally impaired. We show at the single cell level that natural Pf infection induces the development of classical memory B cells (CM) and atypical memory B cells (AtM) that produce broadly neutralizing antibodies against blood stage Pf parasites. CM and AtM contribute to anti-Pf serum IgG production, but only AtM show signs of active antibody secretion. AtM and CM were also different in their IgG gene repertoire, suggesting that they develop from different precursors. The findings provide direct evidence that natural Pf infection leads to the development of protective memory B cell antibody responses and suggest that constant immune activation rather than impaired memory function leads to the accumulation of AtM in malaria. Understanding the memory B cell response to natural Pf infection may be key to the development of a malaria vaccine that induces long-lived protection