TCM-1: a nonlinear dynamical computational model to simulate cellular changes in the T cell system; conceptional design and validation

• Published in: Anticancer research Vol. 23; no. 1A; p. 123
• Main Authors: Krueger, Gerhard R F, Brandt, Michael E, Wang, Guanyu, Buja, L Maximilian
• Format: Journal Article
• Language: English
• Published: Greece 01.01.2003
• Subjects: Adult; CD4-Positive T-Lymphocytes - cytology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - pathology; Cell Differentiation - immunology; Cell Division - immunology; Computer Simulation; Herpesvirus 6, Human; HIV Infections - immunology; HIV-1; HTLV-I Infections - immunology; Human T-lymphotropic virus 1; Humans; Lymphoproliferative Disorders - immunology; Models, Immunological; Nonlinear Dynamics; Roseolovirus Infections - immunology; T-Lymphocytes, Helper-Inducer - cytology; T-Lymphocytes, Helper-Inducer - immunology; T-Lymphocytes, Helper-Inducer - pathology; Virus Diseases - immunology
• ISSN: 0250-7005; 1791-7530

Based upon a previously developed theory of dysregulative lymphoma pathogenesis, a computer model is designed in order to simulate cell changes occurring in disturbances of the T cell immune system and in lymphoproliferative diseases. The model is based upon the concept that factors identified as proliferation factors, differentiation factors and inhibition factors exert a network regulation upon development and function of the T cell system, and that selective disturbances of these factors may lead to hyperplastic, aplastic or neoplastic diseases. The resulting computer model (TCM-1) was validated by comparing it with data from human diseases such as acute HHV-6 (viral) infection, chronic persistent HHV-6 infection, progressive HIV1 infection and HTLV-1 infection, and comparing the simulation results with the actual cell data in the human patients. All these infections target the same T cell population (i.e. CD4 + T helper cells), yet cause different prototypical reactions (hyperplastic, aplastic, neoplastic). The described computer model, which was successfully used to simulate changes in the benign lymphoproliferative disease, Canale-Smith syndrome, will serve as the basis model for further supplementation to accommodate identified factorial influences such as by cytokines, chemokines and others.