COMPARATIVE CELLULAR IMMUNE HOST RESPONSE IN ACUTE VS HEALED LESIONS OF CUTANEOUS LEISHMANIASIS

Authors

  • Simeen Ber Rahman
  • Arfan ul Bari

Abstract

Background: Cutaneous leishmaniasis (CL) has become a major public health problem in
Pakistan and research is now focused to characterize the host's immune response, its clinical
correlation and subsequent implications in management in this disease. This study was done to
evaluate cellular immune host response in patients with active and healed CL and its possible
implications in prevention of disease in susceptibles. Methods: This cross sectional and
comparative study was conducted in Armed Forces Institute of Pathology (AFIP) and Military
Hospital (MH) Rawalpindi (1998-2000). 30 biopsies of active skin lesions and 15 biopsies from
healed lesions, after processing, were studied for various immunophenotype cells by using
monoclonal antibodies. Total and differential T cell counts were recorded in these skin tissues.
Non parametric Kruskal-Wallis Test for one way ANOVA was used to compare the median cell
counts between active, healed and normal skin and p-value <0.05 was considered significant.
Results: The total cell counts, CD3+ cells and CD57+ (NK) cells were found statistically different
(p=<0.001) when active forms of the disease were compared with healed lesions and normal skin
tissue. The difference was not significant (p=>0.05) on comparing healed lesions with normal skin
tissue biopsies except in case of CD3+ cell counts (p=<0.05). However, CD4+, CD8+ and
CD19+(Plasma cells) counts were never seen significant (p=>0.05) on comparison. Conclusion:
NK cells and gamma delta cells seem to be responsible for limitation of the disease and
elimination of the parasite from the lesion in cases of acute cutaneous leishmaniasis.
Keywords: Leishmaniasis, Cutaneous leishmaniasis, Cellular immune host response

References

Mujtaba G, Khalid M. Cutaneous leishmaniasis in Multan,

Pakistan. Int J Dermatol 1998; 37: 843-6.

Raja KM, Khan AA, Hameed A, Rahman SB. Unusual

clinical variants of cutaneous leishmaniasis in Pakistan. Br J

Dermatol.1998: 139: 111-3.

Grimaldi Jr G, Tesh RB. Leishmaniasis of the New World:

current concepts and implications for future research. Clin

Microbiol Review1993; 6: 230-50.

Grevelink SA, Lerner EA. Leishmaniasis. J Am Acad

Dermatol 1996; 34: 257-72.

Lainson R, Shaw JJ. Evolution, classification, and

geographical distribution. In: PetersW, Killick-Kendrick R,

Eds. The leishmaniasis in biology and medicine. San Diego:

Academic Press; 1987: 1-120.

Mitchell GF. Co-evolution of parasites and adaptive immune

response. Parasitology Today 1991;3: A2-5.

Da-Cruz AM, Bittar R, Mattos M, Oliveira-Neto MP,

Nogueira R, Pinho-Ribeiro V, et al. T-cell-mediated immune

responses in patients with cutaneous or mucosal

leishmaniasis: long-term evaluation after therapy. Clin Diagn

Lab Immunol. 2002; 9: 251-6.

Esterre P, Dedat JP, Frenay CC, Chevaller M, Grimaud JA.

Cell population in the lesions of human cutaneous

leishmaniasis: a light microscopical, immuno-histochemical

and ultrastructural study. Virchows Archiv. A Pathol. Anat.

; 421: 239-47.

Ajdary S, Alimohammadian MH, Eslami MB, Kemp K,

Kharazmi A. Comparison of the immune profile of

nonhealing cutaneous Leishmaniasis patients with those with

active lesions and those who have recovered from infection.

Infect Immun 2000;68: 1760-4.

Lemos de Souza V, Ascencao Souza J, Correia Silva TM,

Sampaio Tavares Veras P, Rodrigues de-Freitas LA.

Different Leishmania species determine distinct profiles of

immune and histopathological responses in CBA mice.

Microbes Infect 2000; 2: 1807-15.

Jaroskova L, Selim MM, Vlasin Z and Al-Taqui M. Study of

T cell subset in patients with cutaneous leishmaniasis.

Parasite Immunology 1986; 8: 381-9

Modlin RL, Tapia FJ, Bloom BR, Gallinoto ME, Caste M,

Randon AJ, et al. In situ characterisation of cellular immune

J Ayub Med Coll Abbottabad 2006;18(3)

response in American cutaneous leishmaniasis. Clin Exp

Immunol. 1985; 60: 241-8.

Barral A, Jesus AR, Almeida RP, Carvalho, Barral- Netto M,

Costa JML, et al. Evaluation of T cell subsets in the lesion

infiltrates of human cutaneous and mucocutaneous

leishmaniasis. Parasite Immunology 1987; 9: 487-97.

Ridel P R, Esterre P, Dedat JP, Pradinaud R, Santoro F,

Capron A. Killer cells in human cutaneous leishmaniasis.

Trans R Soc Trop Med Hyg 1988; 82: 223-6.

Lima HC, Vasconcelos AW, David JR, Lerner EA. American

cutaneous leishmaniasis: In situ characterisation of the

cellular immune response with time. Am J Trop Med Hyg

; 50: 743-7.

Nilsen R , Mshana RN. In situ characterisation of the

cutaneous immune response in Ethiopian cutaneous

leishmaniasis. Scan J Immunol 1987; 26: 503-12.

Modlin RL, Pirmez C, Hofman FM, Torigian V, Uyemura K,

Rea TH, et al. Lymphocytes bearing antigen-specific gamma

delta T cells receptors accumulates in human infectious

disease lesions. Nature 1986; 339: 544-8.

Abbas A K, Murphy K M, Sher A. Functional diversity of

helper T lymphocytes. Nature 1996;383: 787-93.

Alaibac M, Morris J, Chu AC. Gamma delta T-cells in

human cutaneous immunology. Int J Clin Lab Res 1997; 27:

-64.

Ridel P R, Esterre P, Dedat JP, Pradinaud R, Santoro F,

Capron A. Killer cells in human cutaneous leishmaniasis.

Trans R Soc Trop Med Hyg 1988; 82: 223-6.

Maasho K, Sanchez F, Schurr E, Hailu A, Akuffo H.

Indications of the protective role of natural killer cells in

human cutaneous leishmaniasis of endemicity. Infect Immun

; 66: 2698-704.

Laurenti MD, Gidlund M, Ura DM, Sinhorini IL, Corbett CE,

Goto H. The role of natural killer cells in the early period of

infection in murine cutaneous leishmaniasis. Braz J Med Biol

Res 1999; 32: 323-5.

Matte C, Olivier M. Leishmania-induced cellular recruitment

during the early inflammatory response: modulation of

proinflammatory mediators. J Infect Dis. 2002; 185: 673-81

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Rahman, S. B., & Bari, A. ul. (2006). COMPARATIVE CELLULAR IMMUNE HOST RESPONSE IN ACUTE VS HEALED LESIONS OF CUTANEOUS LEISHMANIASIS. Journal of Ayub Medical College Abbottabad, 18(3). Retrieved from https://jamc.ayubmed.edu.pk/index.php/jamc/article/view/4243

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Vol. 18 No. 3 (2006): JOURNAL OF AYUB MEDICAL COLLEGE, ABBOTTABAD

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ORIGINAL ARTICLE

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