In this paper, we study two mathematical models, involving delay differential equations, which describe the processes of erythropoiesis and leukopoiesis in the case of maintenance therapy for acute lymphoblastic leukemia. All types of possible equilibrium points were determined, and their stability was analyzed. For some of the equilibrium points, conditions for parameters that imply stability were obtained. When this was not feasible, due to the complexity of the characteristic equation, we discuss the stability through numerical simulations. An important part of the stability study for each model is the examination of the critical case of a zero root of the characteristic equation. The mathematical results are accompanied by biological interpretations.

In this paper the stability of the zero equilibrium of a system with time delay is studied. The critical case of a multiple zero root of the characteristic equation of the linearized system is treated by applying a Malkin type theorem and using a complete Lyapunov-Krasovskii functional. An application to a model for malaria under treatment considering the action of the immune system is presented.

The complex model studied in this paper considers the competition between the populations of healthy and leukemic stem-like short-term and mature leukocytes and the influence of the T-lymphocytes on the evolution of leukemia. Delay differential equations with delay-dependent parameters are used in a modified Mackey-Glass approach, with the consideration of asymmetric division and feedback functions for the action of the immune system. The paper is concerned with analytical conditions for stability of one type of equilibrium point. This will result in parameter values that ensure the local stability, or instability, of the system. The influence of the immune system on the cell populations will also be investigated. Numerical simulations will complete the study.

We introduce a new model that captures the cellular evolution of patients with chronic lymphocytic leukemia who are receiving chemotherapy. As chemotherapy can induce allergic reactions and tumor lysis syndrome, we took into account the process of desensitization and the number of dead leukemic cells in the body. The mathematical model uses delayed-differential equations. Qualitative properties of the solutions are proved, including partial stability with respect to some variables and to the invariant set of positive initial data. Numerical simulations are also used to complete the description of the interplay between the immune system’s function, the chemotherapeutic activity and the allergic reactions caused by the therapy.

This mathematical model delves into the dynamics of the immune system during Chronic Myeloid Leukemia (CML) therapy with imatinib. The focus lies in elucidating the allergic reactions induced by imatinib, specifically its impact on T helper (Th) cells and Treg cells. The model integrates cellular interactions, drug pharmacokinetics, and immune responses to unveil the mechanisms underlying the dominance of Th2 over Th1 and Treg cells, leading to allergic manifestations. Through a system of coupled delay differential equations, the interplay between healthy and leukemic cells, the influence of imatinib on T cell dynamics, and the emergence of allergic reactions during CML therapy are explored.

We present a mathematical model that captures the dynamics of the immune system during allergic reactions. Using delay differential equations, we depict the evolution of T cells, APC_s, and IL₆, considering cell migration between various body compartments. The biological discussions and interpretations within the article revolve around drug desensitization, highlighting one potential application of the model. We conduct stability analysis on certain equilibrium points, demonstrating stability in some cases and only partial stability in others. Numerical simulations validate the theoretical findings.