Sepsis leads to a systemic immune response, and despite the progress of modern medicine, it is still responsible for a high mortality rate. The immune response to sepsis is dependent on the innate and adaptive immune systems. The first line is the innate system, which requires complex and multiple pathways in order to eliminate the invading threats. The adaptive responses start after the innate response. The cell-mediated arm of CD4+ and CD8+ T and B cells is the main responsible for this response. A coordinated cytokine response is essential for the host immune response. A dysregulated response can lead to a hyperinflammatory condition (cytokine storm). This hyperinflammation leads to neutrophils activation and may also lead to organ dysfunction. An imbalance of this response can increase the anti-inflammatory response, leading to compensatory anti-inflammatory response syndrome (CARS), persistent inflammation-immunsupression, catabolism syndrome (PICS), and, above all, an immune paralysis stat. This immune paralysis leads to opportunistic infections, Candida species being one of the emerging microorganisms involved. The host immune response is different for bacterial or Candida sepsis. Immune responses for bacterial and Candida sepsis are described in this paper.