Immune checkpoint blockade (ICB) has changed the paradigm of non-small cell lung cancer (NSCLC) with significant improvements in response rates and durability in disease control [1]. However, as recently observed, checkpoint inhibition-based therapies are associated with a spectrum of adverse events that can cause significant morbidity in select patients [2]. These unique toxicity patterns preclude us from achieving uniform outcomes with ICB. Immune-related adverse events (irAEs) are thought to arise in the context of immune dysregulation secondary to anti-programmed cell death-1 (anti-PD-1) or anti-programmed cell death ligand-1 (anti-PD-L1) therapy. Some commonly observed irAEs after ICB in NSCLC include pneumonitis, transaminitis, thyroiditis, hepatitis, etc.

Interleukin-6 (IL-6) is a pleiotropic cytokine with several critical biological functions one of which is its pro-inflammatory role in the tumor microenvironment [3]. IL-6 signaling is believed to play a vital role in promoting tumorigenesis via activation of STAT-3, a pro-oncogenic transcription factor [4]. C-reactive protein (CRP) is an acute phase protein secreted by hepatocytes in response to inflammatory cytokines such as IL-6 and TNF-a [5]. Recent evidence derived from studies describing cytokine release syndrome (CRS) after chimeric antigen receptor T-cell therapy (CAR-T cell) in leukemia suggests that peripheral blood CRP levels may act as a surrogate for the in vivo IL-6 activity [6]. Taking these factors into account, in an attempt to ascertain the predictive value of CRP as well as its correlation with irAEs in ICB, we initiated a study aimed at trending the CRP levels of patients that were started on second-line ICB therapy with nivolumab [7]. From the data analyzed, we observed an increase in CRP with irAEs compared to baseline and hypothesized that similar to CRS, elevated CRP could likely be secondary to a high IL-6 activity in vivo. As proof of concept, we present a case of immune pneumonitis secondary to atezolizumab, an anti-PD-L1 antibody. We trended patient CRP levels during ICB therapy and managed to obtain cytokine levels at the point of the index irAE, ie, pneumonitis in this case. In addition to steroids, we treated the patient