The protozoan that causes malaria is Plasmodium, which indeed infects and resides within red blood cells (RBCs). However, there are some inaccuracies in the statements provided.
Firstly, while it is true that RBCs do not possess major histocompatibility complex (MHC) molecules and therefore cannot directly present antigens to T cells, other antigen-presenting cells (APCs) such as dendritic cells can capture and present malaria antigens to T cells, initiating an adaptive immune response.
Secondly, although RBCs themselves do not enter lymphoid tissues, the antigens derived from malaria parasites can reach lymphoid tissues through the action of dendritic cells or by being released from damaged RBCs. This allows for interaction with immune cells and the initiation of an adaptive immune response.
Thirdly, complement, which is a part of the immune system that helps in destroying pathogens, can indeed act on RBCs. In some cases of malaria, the complement system can contribute to the destruction of infected RBCs.
Lastly, RBCs do not typically produce cytokines necessary for adaptive immune responses. Cytokines are produced by various immune cells such as T cells, B cells, and macrophages. However, during malaria infection, cytokines are produced by these immune cells as part of the immune response to the parasite.
In summary, while the adaptive immune response to malaria is complex and presents challenges, the statements provided contain some inaccuracies regarding the role of RBCs in antigen presentation, lymphoid tissue interaction, complement-mediated destruction, and cytokine production.