CH. Gastritis
According to Dr. Sattar, in Chronic gastritis , the damage is mediated by T-cells which is type iv hsr. As a consequence of which you get autoantibodies in the blood which are against parietal cells and intrinsic factor, so its useful for diagnosis.
Also in Robbins it says,
"It was initially thought that the autoantibodies to parietal cell components, most prominently the H+,K+-ATPase, or proton pump, and intrinsic factor were involved in the pathogenesis of autoimmune gastritis. However, this is unlikely because neither secreted intrinsic factor nor the luminally oriented proton pump are accessible to circulating antibodies, and passive transfer of these antibodies does not produce gastritis in experimental animals. It is more likely that CD4+ T cells directed against parietal cell components, including the H+,K+-ATPase, are the principal agents of injury. This is supported by the observation that transfer of H+,K+-ATPase-reactive CD4+ T cells into naive mice results in gastritis and production of H+,K+-ATPase autoantibodies. There is no evidence of an autoimmune reaction to chief cells, suggesting that these are lost through gastric gland destruction during autoimmune attack on parietal cells. If autoimmune destruction is controlled by immunosuppression, the glands can repopulate, demonstrating that gastric stem cells survive and are able to differentiate into parietal and chief cells."
But i think if we are considering Pernicious anemia, we should say its type 2 and ch gastritis is type 4.