Persistence of traumatic memories in World War II prisoners of war.

OBJECTIVES: To assess the long-term effects of the prisoner of war (POW) experience on U.S. World War II (WWII) veterans. DESIGN: Exploratory study. SETTING: Participants were recruited through the Hines Veterans Affairs Hospital; a POW reunion in Orlando, Florida; and the WWII veterans periodical, "The QUAN." PARTICIPANTS: One hundred fifty-seven American military veterans who were former WWII POWs. MEASURMENTS: Participants completed a mailed survey describing their POW experiences, POW effects on subsequent psychological and physical well-being, and ways in which these experiences shaped major decisions in their lives. RESULTS: Participants from the European and Pacific theaters reported that their captivity during WWII affected their long-term emotional well-being. Both groups reported high rates of reflection, dreaming, and flashbacks pertaining to their POW experiences, but Pacific theater POWs did so at higher rates in the present than in the past. Large portions of both groups reported greater rumination on POW experiences after retirement. Finally, 16.6% of participants met the requirements of a current, clinical diagnosis of posttraumatic stress disorder (PTSD) based on the Mississippi PTSD scale, with PTSD rates in Pacific theater POWs (34%) three times those of European theater POWs (12%). CONCLUSION: Traumatic memories and clinical levels of PTSD persist for WWII POWs as long as 65 years after their captivity. Additionally, rumination about these experiences, including flashbacks and persistent nightmares, may increase after retirement, particularly for those held in the Pacific theater. These findings inform the current therapeutic needs of this elderly population and future generations of POWs from other military conflicts.

Aging affects initiation and continuation of T cell proliferation.

Aging is associated with a decline in immune responses, particularly within the T cell compartment. While the expansion of specific T cells in response to virus infections is consistently decreased in aged mice, the differences in T cell activation between young and aged mice as demonstrated in each round of proliferation remain poorly defined. In the present study, we utilized the T cell mitogen, ConA, to explore if fewer T cells of aged mice initiate proliferation upon mitogen stimulation or if similar numbers of T cells of aged mice begin proliferation but undergo fewer rounds of division. We also examined whether these age-associated changes in proliferation are reflected by differences in T cell activation by comparing activation markers (CD25, CD69, CD44, and CD62L) on T cells of young and aged mice at each round of proliferation. Not only was the kinetics of the expression of these markers greatly different between young and aged mice on the entire CD8 T cell population, but also at each round of proliferation. Our results demonstrate that a larger percentage of CD8 T cells of aged mice do not proliferate at all upon stimulation. Of the CD8 T cells of aged mice that do proliferate, a larger percentage start later and stop sooner. These results suggest that multiple levels of alteration may need to be considered when trying to maximize the immune response of aged individuals.

Depletion of T cells by type I interferon: differences between young and aged mice.

Type I IFN (IFN-I or IFN-alphabeta) plays an important role in the innate immune response against viral infection. Here we report that a potent inducer of IFN-alphabeta, polyinosinic-polycytidylic acid [poly(I:C)], led to the depletion of T cells in young, but not aged mice, and that this depletion was limited to central memory, but not effector memory, T cells. Although early activation of T cells in vivo by poly(I:C), as demonstrated by CD69, was not impaired with aging, the expression of active caspase-3 was higher in young compared with aged mice. This depletion of T cells and induction of active caspase-3 in young mice and of CD69 in both young and aged mice by poly(I:C) were blocked by anti-IFN-alphabeta Ab. Although poly(I:C) stimulated lower circulating levels of IFN-alphabeta in aged mice, administration of IFN-alphabeta after poly(I:C) did not induce depletion of T cells in aged mice. These results indicate that IFN-alphabeta plays a critical role in the depletion of T cells of young mice, and further suggest that the lower level of functional IFN-alphabeta and decreased induction of active caspase-3 in T cells of aged mice after poly(I:C) may be responsible for the increased resistance of T cells of aged mice to depletion.