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Neutrophil deficiency led to reduced macrophage infiltration and a striking increase in nonconventional CD4\n                    <jats:sup>\u2212<\/jats:sup>\n                    CD8\n                    <jats:sup>\u2212<\/jats:sup>\n                    (double\u2010negative) \u03b1\u03b2 and \u03b3\u03b4 T\u00a0cell numbers, peaking at Day 3 postinjury. In exploring the underlying mechanisms, we identified previously unrecognized cellular and tissue alterations, including bone marrow erythroid insufficiency and compensatory extramedullary hematopoiesis accompanied by splenomegaly. Using a thioglycolate\u2010induced peritonitis model, we further demonstrated that elevated T\u2010cell numbers reflect a general inflammatory response in neutrophil\u2010deficient mice. Our findings suggest that this model provides a valuable platform for investigating the properties and functions of rare nonconventional T\u00a0cells in tissue injury and diverse inflammatory conditions.\n                    <jats:boxed-text content-type=\"box\" position=\"anchor\">\n                      <jats:caption>\n                        <jats:title>Impact statement<\/jats:title>\n                      <\/jats:caption>\n                      <jats:p>Our studies demonstrate that neutrophil\u2010deficient mice may provide a valuable model for investigating the roles and characteristics of non\u2010conventional T\u00a0cells in tissue inflammation and repair.<\/jats:p>\n                    <\/jats:boxed-text>\n                  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