Cerebral inflammation is a promising therapeutic target for ischaemic stroke. After ischaemic stroke, inflammatogenic self-molecules, which originate from damaged brain tissue due to ischaemia, activate infiltrating immune cells (neutrophils, macrophages and lymphocytes) and thereby trigger sterile inflammation. Innate immunity plays the central role in sterile inflammation at the acute phase of brain ischaemia, although immune response by T lymphocytes (innate or acquired immunity) is also implicated in inflammation at the subacute phase, which sustains ischaemic brain damage. In the recovery phase, infiltrating macrophages remove the damage-associated molecular patterns (DAMPs) from the ischaemic brain. These pro-resolving myeloid cells also produce neurotrophic factors involved in neural repair. Through a series of inflammatory mechanisms activated by ischaemic stroke, various immune cells change their functions from inflammation to repair in a precise process. In order to establish therapeutic strategies for the improvement of neurological deficits after ischaemic stroke, it is necessary to clarify the detailed molecular and cellular mechanisms of sterile inflammation after ischaemic brain injury.