Autoimmune pre-disease

Katja Bieber; Jennifer E Hundt; Xinhua Yu; Marc Ehlers; Frank Petersen; Christian M Karsten; Jörg Köhl; Khalaf Kridin; Kathrin Kalies; Anika Kasprick; Stephanie Goletz; Jens Y Humrich; Rudolf A Manz; Axel Künstner; Christoph M Hammers; Reza Akbarzadeh; Hauke Busch; Christian D Sadik; Tanja Lange; Hanna Grasshoff; Alexander M Hackel; Jeanette Erdmann; Inke König; Walter Raasch; Mareike Becker; Anja Kerstein-Stähle; Peter Lamprecht; Gabriela Riemekasten; Enno Schmidt; Ralf J Ludwig

doi:10.1016/j.autrev.2022.103236

Autoimmune pre-disease

Standard

Autoimmune pre-disease. / Bieber, Katja; Hundt, Jennifer E; Yu, Xinhua; Ehlers, Marc; Petersen, Frank; Karsten, Christian M; Köhl, Jörg; Kridin, Khalaf; Kalies, Kathrin; Kasprick, Anika; Goletz, Stephanie; Humrich, Jens Y; Manz, Rudolf A; Künstner, Axel; Hammers, Christoph M; Akbarzadeh, Reza; Busch, Hauke; Sadik, Christian D; Lange, Tanja; Grasshoff, Hanna; Hackel, Alexander M; Erdmann, Jeanette; König, Inke; Raasch, Walter; Becker, Mareike; Kerstein-Stähle, Anja; Lamprecht, Peter; Riemekasten, Gabriela; Schmidt, Enno; Ludwig, Ralf J.

In: AUTOIMMUN REV, Vol. 22, No. 2, 02.2023, p. 103236.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Bieber, K, Hundt, JE, Yu, X, Ehlers, M, Petersen, F, Karsten, CM, Köhl, J, Kridin, K, Kalies, K, Kasprick, A, Goletz, S, Humrich, JY, Manz, RA, Künstner, A, Hammers, CM, Akbarzadeh, R, Busch, H, Sadik, CD, Lange, T, Grasshoff, H, Hackel, AM, Erdmann, J, König, I, Raasch, W, Becker, M, Kerstein-Stähle, A, Lamprecht, P, Riemekasten, G, Schmidt, E & Ludwig, RJ 2023, 'Autoimmune pre-disease', AUTOIMMUN REV, vol. 22, no. 2, pp. 103236. https://doi.org/10.1016/j.autrev.2022.103236

APA

Bieber, K., Hundt, J. E., Yu, X., Ehlers, M., Petersen, F., Karsten, C. M., Köhl, J., Kridin, K., Kalies, K., Kasprick, A., Goletz, S., Humrich, J. Y., Manz, R. A., Künstner, A., Hammers, C. M., Akbarzadeh, R., Busch, H., Sadik, C. D., Lange, T., ... Ludwig, R. J. (2023). Autoimmune pre-disease. AUTOIMMUN REV, 22(2), 103236. https://doi.org/10.1016/j.autrev.2022.103236

Vancouver

Bieber K, Hundt JE, Yu X, Ehlers M, Petersen F, Karsten CM et al. Autoimmune pre-disease. AUTOIMMUN REV. 2023 Feb;22(2):103236. https://doi.org/10.1016/j.autrev.2022.103236

Bibtex

@article{0d4dc7c9fb64422da5ed539c8a118e09,

title = "Autoimmune pre-disease",

abstract = "Approximately 5% of the world-wide population is affected by autoimmune diseases. Overall, autoimmune diseases are still difficult to treat, impose a high burden on patients, and have a significant economic impact. Like other complex diseases, e.g., cancer, autoimmune diseases develop over several years. Decisive steps in the development of autoimmune diseases are (i) the development of autoantigen-specific lymphocytes and (often) autoantibodies and (ii) potentially clinical disease manifestation at a later stage. However, not all healthy individuals with autoantibodies develop disease manifestations. Identifying autoantibody-positive healthy individuals and monitoring and inhibiting their switch to inflammatory autoimmune disease conditions are currently in their infancy. The switch from harmless to inflammatory autoantigen-specific T and B-cell and autoantibody responses seems to be the hallmark for the decisive factor in inflammatory autoimmune disease conditions. Accordingly, biomarkers allowing us to predict this progression would have a significant impact. Several factors, such as genetics and the environment, especially diet, smoking, exposure to pollutants, infections, stress, and shift work, might influence the progression from harmless to inflammatory autoimmune conditions. To inspire research directed at defining and ultimately targeting autoimmune predisease, here, we review published evidence underlying the progression from health to autoimmune predisease and ultimately to clinically manifest inflammatory autoimmune disease, addressing the following 3 questions: (i) what is the current status, (ii) what is missing, (iii) and what are the future perspectives for defining and modulating autoimmune predisease.",

author = "Katja Bieber and Hundt, {Jennifer E} and Xinhua Yu and Marc Ehlers and Frank Petersen and Karsten, {Christian M} and J{\"o}rg K{\"o}hl and Khalaf Kridin and Kathrin Kalies and Anika Kasprick and Stephanie Goletz and Humrich, {Jens Y} and Manz, {Rudolf A} and Axel K{\"u}nstner and Hammers, {Christoph M} and Reza Akbarzadeh and Hauke Busch and Sadik, {Christian D} and Tanja Lange and Hanna Grasshoff and Hackel, {Alexander M} and Jeanette Erdmann and Inke K{\"o}nig and Walter Raasch and Mareike Becker and Anja Kerstein-St{\"a}hle and Peter Lamprecht and Gabriela Riemekasten and Enno Schmidt and Ludwig, {Ralf J}",

year = "2023",

month = feb,

doi = "10.1016/j.autrev.2022.103236",

language = "English",

volume = "22",

pages = "103236",

journal = "AUTOIMMUN REV",

issn = "1568-9972",

publisher = "Elsevier",

number = "2",

}

RIS

TY - JOUR

T1 - Autoimmune pre-disease

AU - Bieber, Katja

AU - Hundt, Jennifer E

AU - Yu, Xinhua

AU - Ehlers, Marc

AU - Petersen, Frank

AU - Karsten, Christian M

AU - Köhl, Jörg

AU - Kridin, Khalaf

AU - Kalies, Kathrin

AU - Kasprick, Anika

AU - Goletz, Stephanie

AU - Humrich, Jens Y

AU - Manz, Rudolf A

AU - Künstner, Axel

AU - Hammers, Christoph M

AU - Akbarzadeh, Reza

AU - Busch, Hauke

AU - Sadik, Christian D

AU - Lange, Tanja

AU - Grasshoff, Hanna

AU - Hackel, Alexander M

AU - Erdmann, Jeanette

AU - König, Inke

AU - Raasch, Walter

AU - Becker, Mareike

AU - Kerstein-Stähle, Anja

AU - Lamprecht, Peter

AU - Riemekasten, Gabriela

AU - Schmidt, Enno

AU - Ludwig, Ralf J

PY - 2023/2

Y1 - 2023/2

N2 - Approximately 5% of the world-wide population is affected by autoimmune diseases. Overall, autoimmune diseases are still difficult to treat, impose a high burden on patients, and have a significant economic impact. Like other complex diseases, e.g., cancer, autoimmune diseases develop over several years. Decisive steps in the development of autoimmune diseases are (i) the development of autoantigen-specific lymphocytes and (often) autoantibodies and (ii) potentially clinical disease manifestation at a later stage. However, not all healthy individuals with autoantibodies develop disease manifestations. Identifying autoantibody-positive healthy individuals and monitoring and inhibiting their switch to inflammatory autoimmune disease conditions are currently in their infancy. The switch from harmless to inflammatory autoantigen-specific T and B-cell and autoantibody responses seems to be the hallmark for the decisive factor in inflammatory autoimmune disease conditions. Accordingly, biomarkers allowing us to predict this progression would have a significant impact. Several factors, such as genetics and the environment, especially diet, smoking, exposure to pollutants, infections, stress, and shift work, might influence the progression from harmless to inflammatory autoimmune conditions. To inspire research directed at defining and ultimately targeting autoimmune predisease, here, we review published evidence underlying the progression from health to autoimmune predisease and ultimately to clinically manifest inflammatory autoimmune disease, addressing the following 3 questions: (i) what is the current status, (ii) what is missing, (iii) and what are the future perspectives for defining and modulating autoimmune predisease.

AB - Approximately 5% of the world-wide population is affected by autoimmune diseases. Overall, autoimmune diseases are still difficult to treat, impose a high burden on patients, and have a significant economic impact. Like other complex diseases, e.g., cancer, autoimmune diseases develop over several years. Decisive steps in the development of autoimmune diseases are (i) the development of autoantigen-specific lymphocytes and (often) autoantibodies and (ii) potentially clinical disease manifestation at a later stage. However, not all healthy individuals with autoantibodies develop disease manifestations. Identifying autoantibody-positive healthy individuals and monitoring and inhibiting their switch to inflammatory autoimmune disease conditions are currently in their infancy. The switch from harmless to inflammatory autoantigen-specific T and B-cell and autoantibody responses seems to be the hallmark for the decisive factor in inflammatory autoimmune disease conditions. Accordingly, biomarkers allowing us to predict this progression would have a significant impact. Several factors, such as genetics and the environment, especially diet, smoking, exposure to pollutants, infections, stress, and shift work, might influence the progression from harmless to inflammatory autoimmune conditions. To inspire research directed at defining and ultimately targeting autoimmune predisease, here, we review published evidence underlying the progression from health to autoimmune predisease and ultimately to clinically manifest inflammatory autoimmune disease, addressing the following 3 questions: (i) what is the current status, (ii) what is missing, (iii) and what are the future perspectives for defining and modulating autoimmune predisease.

U2 - 10.1016/j.autrev.2022.103236

DO - 10.1016/j.autrev.2022.103236

M3 - SCORING: Review article

C2 - 36436750

VL - 22

SP - 103236

JO - AUTOIMMUN REV

JF - AUTOIMMUN REV

SN - 1568-9972

IS - 2

ER -