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The control of infections by the vertebrate adaptive immune system requires careful modulation to optimize defense and minimize harm to the host. The Fc receptor-like (<i>FCRL</i>) genes encode immunoregulatory molecules homologous to the receptors for the Fc portion of immunoglobulin (FCR). To date, nine different genes (<i>FCRL1–6</i>, <i>FCRLA</i>, <i>FCRLB</i> and <i>FCRLS</i>) have been identified in mammalian organisms. <i>FCRL6</i> is located at a separate chromosomal position from the <i>FCRL1-5</i> locus, has conserved synteny in mammals and is situated between the <i>SLAMF8</i> and <i>DUSP23</i> genes. Here, we show that this three gene block underwent repeated duplication in <i>Dasypus novemcinctus</i> (nine-banded armadillo) resulting in six <i>FCRL6</i> copies, of which five appear functional. Among 21 mammalian genomes analyzed, this expansion was unique to <i>D. novemcinctus</i>. Ig-like domains that derive from the five clustered <i>FCRL6</i> functional gene copies show high structural conservation and sequence identity. However, the presence of multiple non-synonymous amino acid changes that would diversify individual receptor function has led to the hypothesis that <i>FCRL6</i> endured subfunctionalization during evolution in <i>D. novemcinctus</i>. Interestingly, <i>D. novemcinctus</i> is noteworthy for its natural resistance to the <i>Mycobacterium leprae</i> pathogen that causes leprosy. Because <i>FCRL6</i> is chiefly expressed by cytotoxic T and NK cells, which are important in cellular defense responses against <i>M. leprae</i>, we speculate that <i>FCRL6</i> subfunctionalization could be relevant for the adaptation of <i>D. novemcinctus</i> to leprosy. These findings highlight the species-specific diversification of <i>FCRL</i> family members and the genetic complexity underlying evolving multigene families critical for modulating adaptive immune protection.