Candida albicans (C. albicans), a conditional pathogenic fungus, is widespread in nature and can live in symbiosis with organisms in small quantities. When the normal microflora is imbalanced, the epithelial barrier is disrupted or the immune system becomes dysfunctional, C. albicans can change from commensal to pathogenic pathogen, causing both superficial and life-threatening systemic infections with no effective treatment. The morbidity and mortality of invasive Candida infections in perioperative patients are high due to underlying chronic diseases, immune deficiencies, and pathophysiological disorders. C-type lectin receptors (CLRs) are the main pattern-recognition receptors for fungal activation of innate immunity and host defense. Upon binding to ligands, CLRs induce multiple signal transduction cascades followed by activation of nuclear factor kappa B through spleen tyrosine kinase - and caspase recruitment domain containing protein 9-dependent pathways. Analyzing the effects of regulatory CLR-induced signaling cascades on host immune cells is critical for understanding the molecular mechanism in regulating antifungal immunity. As one of the core factors in host innate immune regulation, protein post-translational modifications regulate the strength of immune effects by modulating protein conformation, stability, affinity, subcellular localization, etc. This makes the post-translational modification sites promising as potential targets for modulating antifungal immunity. This review primarily described the study progress of post-translational modifications in controlling CLR-induced signaling cascades throughout the process of innate immunity against C. albicans. We aim to provide better understanding of these mechanisms and aid in the identification and development of biomarkers and drug targets for invasive candidiasis.