Abstract

Research connects stressful events with altered immune regulation, but the role of subjective stress is uncertain. Using a longitudinal design, we provide a statistically powerful test of the relationship between subjective stress (perceived stress, emotional distress) and immunity (T cell blastogenesis, natural killer cell cytotoxicity, [NKCC]) as individuals adjust to a severe stressor, a cancer diagnosis and its treatments. Women with regional breast cancer (N = 113) were assessed at diagnosis/surgery and reassessed 4, 8, 12, and 18 months later. Latent growth curve analysis tested two hypotheses: (1) initial levels of subjective stress will correlate inversely with initial levels of immunity, and (2) rate of change in subjective stress will correlate inversely with rate of change in immunity. As predicted by Hypothesis 1, participants with high initial subjective stress showed poor initial blastogenesis. As predicted by Hypothesis 2, participants exhibiting an early, rapid decline in subjective stress also showed rapid improvement in NKCC. Follow-up analyses revealed perceived stress to be strongly related to immune function, while emotional distress was not. This is the first study to investigate trajectories in stress and immunity during recovery from a major stressor. Results imply that NK and T cells are sensitive to different aspects of the stress response. While T cell blastogenesis correlated with initial (peak) subjective stress, NKCC correlated with change (improvement) in subjective stress. These data highlight the importance of subjective stress, particularly stress appraisals, in the immune response to a major stressor.

Keywords: Stress; Immunity; Psychoneuroimmunology; Breast cancer; Lymphocytes; T cell blastogenesis; Natural killer cell cytotoxicity; Latent growth curve analysis; Individual differences

Article Outline

1. Introduction

1.1. Stress and immunity in the context of cancer

2. Method

2.1. Participants and procedures

2.2. Measures

2.2.1. Subjective stress

2.2.2. Immune function

2.2.2.1. Quantification of immune cells

2.2.2.2. Natural killer cell cytotoxicity

2.2.2.3. Blastogenic response to phytohemagluttinin (PHA) and concanavalin A (Con A)

2.2.3. Demographic, prognostic, and treatment variables

2.3. Analytic strategy

3. Results

3.1. Data availability

3.2. Latent curve analysis

3.2.1. Preliminary analyses

3.2.2. Step 1: Developing univariate models

3.2.3. Step 2: Combining models into joint trajectory models

3.2.4. Step 3: The introduction of controls

4. Discussion

Acknowledgements

References

This research was conducted in the Departments of Psychology and Surgery, and the Comprehensive Cancer Center of the Ohio State University; and Primetrics, Inc., Columbus, OH. This manuscript was based on a dissertation by the first author (LMT).