NR4A1-3 receptors are required in inflammatory disease initiation and progression, where they function as early response regulators, controlling the extent of the inflammatory response and promoting inflammatory resolution. NR4A receptor activity controls inflammatory processes in several diseases characterized by chronic inflammation including rheumatoid arthritis (RA) and atherosclerosis. Studies indicate that cell-type and cellular microenvironment can alter NR4A1-3 receptor activity and influence their biological roles. Thus, the study of appropriate in vivo models of inflammatory disease is important to ascertain their cell- and tissue-specific functional roles. Here we describe immunohistochemical approaches optimized to study the expression patterns of NR4A nuclear receptors in inflamed synovium tissues obtained from patients diagnosed with RA and mouse models of inflammatory joint disease.