Granulocyte recruitment to the pulmonary compartment is a hallmark of progressive tuberculosis (TB). This process is well-documented to promote immunopathology, but can also enhance the replication of the pathogen. Both the specific granulocytes responsible for increasing mycobacterial burden and the underlying mechanisms remain obscure. We report that the known immunomodulatory effects of these cells, such as suppression of protective T-cell responses, play a limited role in altering host control of mycobacterial replication in susceptible mice. Instead, we find that the adaptive immune response preferentially restricts the burden of bacteria within monocytes and macrophages compared to granulocytes. Specifically, mycobacteria within inflammatory lesions are preferentially found within long-lived granulocytes that express intermediate levels of the Ly6G marker and low levels of antimicrobial genes. These cells progressively accumulate in the lung and correlate with bacterial load and disease severity, and the ablation of Ly6G-expressing cells lowers mycobacterial burden. These observations suggest a model in which dysregulated granulocytic influx promotes disease by creating a permissive intracellular niche for mycobacterial growth and persistence.

粒细胞募集到肺室是进行性结核病 (TB) 的标志。这个过程被充分证明可以促进免疫病理学，但也可以增强病原体的复制。负责增加分枝杆菌负担的特定粒细胞及其潜在机制仍然不清楚。我们报告说，这些细胞的已知免疫调节作用（例如抑制保护性 T 细胞反应）在改变宿主对易感小鼠分枝杆菌复制的控制方面发挥的作用有限。相反，我们发现与粒细胞相比，适应性免疫反应优先限制单核细胞和巨噬细胞内细菌的负担。具体来说，炎性病变内的分枝杆菌优先在长寿粒细胞中发现，这些粒细胞表达中等水平的 Ly6G 标记和低水平的抗菌基因。这些细胞逐渐积聚在肺部并与细菌负荷和疾病严重程度相关，并且 Ly6G 表达细胞的消融降低了分枝杆菌负荷。这些观察结果表明了一个模型，在该模型中，失调的粒细胞流入通过为分枝杆菌生长和持久性创造一个允许的细胞内生态位来促进疾病。